| disease | Hypertension |
| alias | High Blood Pressure, Hypertension |
Hypertension is one of the most common cardiovascular diseases and is closely related to major fatal conditions such as coronary heart disease and cerebrovascular diseases. Therefore, countries worldwide place great emphasis on research into the pathogenesis and clinical prevention of hypertension.
bubble_chart Epidemiology
The prevalence of hypertension varies significantly across different regions of the world. It is generally higher in European and American countries compared to Asian and African nations, and higher in industrialized countries than in developing ones. According to data from the WHO MONICA project, the prevalence of hypertension among adults (aged 35–64) in Europe and America exceeds 20%. Even within the same country, prevalence rates can differ among ethnic groups. For example, the prevalence of hypertension among African Americans is approximately twice that of white Americans.
In China, the incidence of hypertension is lower than in Western countries but has been steadily increasing. Using the threshold of blood pressure above 140/90 mmHg to estimate the prevalence among individuals aged 15 and older, the national average prevalence in 1959, based on a survey of 739,204 people across 13 provinces and cities, was 5.11%, with Shanghai reporting 6.96%. By 1979, a survey of 4,012,128 people across 29 provinces, municipalities, and autonomous regions showed the average prevalence had risen to 7.73%, with Shanghai at 7.89%. By 1991, the national average had climbed to 11.88%, with Shanghai reaching 12.69%. Although these figures include borderline and secondary hypertension, the consistent criteria and long time span make the data highly comparable. The MONICA project in China (1988–1989) surveyed the prevalence of confirmed hypertension among individuals aged 35–64. Among men, the highest prevalence was in Jilin Province at 25.8%, while the lowest was in Mianyang, Sichuan, at 4.9%. Among women, the highest was in Shenyang at 24.3%, and the lowest was in Fuzhou at 6.3%. Compared to data from 1984–1986, most northern cities showed an increase in prevalence, with Shenyang women experiencing the largest rise—an increase of 5.7%. These findings reveal significant regional disparities in hypertension prevalence across China. The northeastern and northern regions have higher rates than the southwestern and southeastern regions, and the eastern regions surpass the western regions. These differences may be linked to variations in salt intake, obesity rates, and climatic factors. In recent years, rural areas have also seen rising prevalence rates. For instance, confirmed hypertension prevalence in rural Beijing suburbs increased from 8.7% in 1979 to 9.6% in 1991. The difference in prevalence between genders is minimal, with young men slightly more affected than young women, while middle-aged and older women show slightly higher rates than their male counterparts.
bubble_chart EtiologyThe etiology of this disease has not been fully elucidated. It is currently believed to result from the decompensation of normal blood pressure regulation mechanisms due to the combined effects of various acquired factors on a certain genetic basis. The following factors may be related to its pathogenesis.
(1) Heredity: The onset of hypertension exhibits significant familial aggregation. Children or adolescents with normotensive parents who both have hypertension show significantly higher plasma concentrations of norepinephrine and dopamine compared to a control group without a family history of hypertension, and they also have a higher likelihood of developing hypertension later in life. Domestic surveys have found that individuals with one hypertensive parent have a 1.5 times higher incidence of hypertension compared to those without a family history, while those with both parents having hypertension have a 2–3 times higher incidence. Biological children of hypertensive patients are more prone to developing hypertension than adopted children, even when raised in the same environment. Animal experiments have successfully bred hereditary hypertensive rat strains (SHR), and molecular genetic studies have achieved gene-transferred hypertensive animals. These findings collectively suggest the role of genetic factors.
(2) Diet:
1. Salts: The most closely related to hypertension is Na+. The average blood pressure level in populations correlates with salt intake. In regions with high salt consumption, reducing daily salt intake can lower blood pressure. Some reports indicate a positive correlation between hypertension prevalence and nocturnal urinary sodium content, though conflicting opinions exist, possibly due to differences between salt-sensitive and non-salt-sensitive subgroups within hypertensive populations. High sodium may promote hypertension by increasing sympathetic tone and peripheral vascular resistance. Insufficient dietary intake of K+
2. Fatty acids and amino acids: Reducing total fat intake, increasing unsaturated fatty acids, and decreasing saturated fatty acids can lower the average blood pressure in populations. Animal experiments have shown that consuming sulfur-containing amino acids from fish proteins can prevent blood pressure elevation.
3. Alcohol consumption: Long-term alcohol consumption is associated with an increased prevalence of hypertension, proportional to the amount consumed. This may be related to alcohol-induced elevations in corticosteroid and catecholamine levels.
(3) Occupation and environment: Epidemiological data suggest that individuals engaged in highly attention-demanding work, long-term mental stress, or prolonged exposure to environmental noise and adverse visual stimuli are more prone to hypertension.
(4) Others: Smoking and obesity are associated with a higher prevalence of hypertension.
Cardiac output and peripheral vascular resistance are the two major factors influencing systemic arterial blood pressure. The former is determined by myocardial contractility and circulating blood volume, while the latter is affected by the caliber of resistance vessels, compliance, blood viscosity, etc. The compliance of arterial walls also influences blood pressure levels. The interplay of these various factors, under the regulation of systemic and local neural and humoral factors, continuously fluctuates to maintain the dynamic equilibrium of blood pressure, physiological fluctuations, and stress responses. Acute blood pressure regulation is primarily achieved through baroreceptors located in the carotid sinus and aortic arch. When blood pressure rises, increased afferent impulses from these receptors lead to decreased sympathetic activity and increased vagal tone, thereby lowering blood pressure. Additionally, low-pressure receptors in the atria and pulmonary veins, chemoreceptors in the carotid and aortic bodies, and the central ischemic response also participate in acute blood pressure regulation. Chronic blood pressure regulation is mainly achieved by influencing circulating blood volume through water balance, with the kidneys' regulation of blood volume and the renin-angiotensin-aldosterone system playing key roles. If these regulatory mechanisms become decompensated, leading to increased systemic vascular resistance or (and) increased circulating blood volume, hypertension develops. The pathogenesis of hypertension includes:
The nervous system plays a crucial role in blood pressure regulation. The medullary vasomotor center includes pressor, depressor, and sensory areas, which, with the participation of the pons, hypothalamus, and higher central nuclei, govern vascular regulation. According to the neurogenic theory, hypertension may arise from increased vasoconstrictor impulses from various central levels, enhanced vasoconstrictor signals from receptors, or excessive responsiveness of resistance vessels to neurotransmitters. The heightened activity of the sympathetic nervous system is central to this process, mediated by the release of catecholamine neurotransmitters, particularly norepinephrine, which induces arteriolar constriction. Chronic hypertensive perfusion leads to structural reinforcement, causing vascular smooth muscle proliferation, hypertrophy, and wall thickening with reduced lumen diameter. This, along with induced membrane electrical activity in vascular wall cells, enhances vasoconstrictor responses. Additionally, sympathetic stimulation of renal juxtaglomerular cells increases renin release, sustaining the hypertensive state.
(II) Imbalance of the Renin-Angiotensin-Aldosterone (RAA) System Renal ischemia stimulates the juxtaglomerular cells on the afferent arterioles of the glomerulus to secrete renin. Renin acts on angiotensinogen synthesized by the liver to form angiotensin I (Ang I), which is then converted to angiotensin II (Ang II) by the activating action of angiotensin-converting enzyme (ACE, also known as kininase II) in tissues such as the lungs and kidneys. Ang II is further transformed into Ang III by the enzyme-mediated removal of an aspartic acid residue. In the RAA system, Ang II is the most critical component, exhibiting potent vasoconstrictive effects. Its pressor activity is approximately 10 to 40 times stronger than that of adrenaline. Additionally, Ang II stimulates the zona glomerulosa of the adrenal cortex to secrete aldosterone, promoting water and sodium retention. It also excites sympathetic ganglia to increase norepinephrine secretion and enhances the activity of specific receptors, thereby elevating blood pressure. Furthermore, Ang II exerts negative feedback to inhibit renin secretion by the kidneys and stimulates the kidneys to secrete prostaglandins. Hypertension arises when the RAA system becomes dysfunctional. Since renin is primarily produced in the kidneys, the renal theory of hypertension pathogenesis was previously proposed. However, only a minority of hypertensive patients exhibit elevated plasma renin levels. Recent studies have identified the presence of the renin-angiotensin system in tissues such as vascular walls, the heart, the central nervous system, and the renal cortex and medulla. These tissue-based systems may play a significant role in the pathogenesis of normal-renin and low-renin hypertension, as well as in the target organ damage associated with hypertension.
(3) Genetic Theory Epidemiological studies, animal experiments, and molecular-cellular level research all suggest the role of genetics in the pathogenesis of hypertension. A significant proportion of hypertensive patients have a family history of the condition, with the blood pressure levels of their direct relatives being higher than those of non-direct relatives of the same age. Children with both parents having hypertension face a greater risk of developing the disease. Animal experiments have long identified the SHR (spontaneously hypertensive rat) strain, strongly implicating genetic factors. Molecular biology research has proposed the "membrane theory" for hypertension pathogenesis, suggesting that hypertensive patients inherit ion transport dysfunction in tissue cell membranes. Particularly when sodium intake increases, Na+ cannot be effectively expelled from cells, leading to Na+ retention in vascular smooth muscle cells. This triggers Na+-Ca++ exchange, increasing intracellular Ca++ levels. Additionally, membrane depolarization elevates excitability, ultimately causing vasoconstriction and increased peripheral resistance—a phenomenon also observed in patients' relatives. Hypertensive patients often exhibit specific tissue-related antigen types, such as HLA-B15, HLA-B8, and HLA-B12.
These findings collectively highlight the role of genetic factors in hypertension pathogenesis. Current research indicates that a single genetic factor is unlikely to cause hypertension; rather, this inherited predisposition arises from multiple genetic variants, with acquired factors playing a significant role in its development.
(4) Excessive Dietary Sodium Theory Extensive experimental, clinical, and epidemiological data confirm the close relationship between sodium metabolism and hypertension. Populations in regions with high salt intake, such as native Japanese, exhibit high hypertension prevalence rates, whereas those in low-salt intake regions, like Alaskan Eskimos, rarely develop hypertension. Restricting sodium intake can improve hypertension, and diuretics that increase sodium excretion can also reduce elevated blood pressure. Renal vascular hypertension worsens with high sodium intake and improves with reduced sodium. The administration of deoxycorticosterone induces hypertension only when combined with salt intake. Hypertension caused by adrenal cortical hyperplasia also requires sodium involvement. Postmortem studies show that hypertensive patients and animals have higher sodium and water content per unit volume of dry kidney tissue compared to non-hypertensive individuals. Sodium retention increases extracellular fluid volume, raising cardiac output; elevated water content in small vessel walls increases peripheral resistance; and changes in intracellular-to-extracellular sodium concentration ratios may enhance small vessel tension—all potential pathological mechanisms. However, laboratory and clinical studies reveal that altering salt intake and blood sodium levels affects blood pressure in only a subset of individuals, suggesting that dietary salt's pathogenic role is conditional. It primarily impacts those with inherited sodium transport defects that make them salt-sensitive.
(5) Hyperinsulinemia In recent years, the relationship between hyperinsulinemia and hypertension has garnered attention. Observations show that fasting insulin levels are significantly higher in hypertensive patients, indicating insulin resistance. Individuals with impaired glucose tolerance have a markedly higher incidence of hypertension. Hyperinsulinemia is often accompanied by hypertriglyceridemia and low HDL cholesterol, commonly seen in obese individuals. Animal experiments also confirm insulin resistance in SHR models.
Hyperinsulinemia may lead to hypertension by activating cellular Na+-K+ATPase, thereby increasing intracellular Na+ concentration, promoting sodium retention, reducing Ca2+-ATPase activity to elevate intracellular calcium levels and increase vascular resistance, as well as enhancing sympathetic nervous activity. However, not all individuals with hyperinsulinemia develop hypertension, and vice versa. The relationship between the two requires further research.
(6) Others The prostaglandin system is closely related to the renin-angiotensin-aldosterone system. Some believe that hypertension may be associated with insufficient synthesis of vasodilatory prostaglandins A or E by the renal medulla. The kallikrein-kinin system is also related to the renin-angiotensin-aldosterone system. Angiotensin-converting enzyme promotes the degradation of kinins, causing their vasodilatory effects to disappear and blood pressure to rise. Smoking, excessive alcohol consumption, and excessive carbohydrate intake leading to obesity also predispose individuals to hypertension.
In recent years, the role of peptide substances such as vasopressin and endothelin in causing hypertension has also drawn attention.
Traditional Chinese medicine holds that this disease is related to the "liver" and "kidney" organs. An abnormal exuberance of yin or yang in the constitution, or a deficiency, along with dysfunction of qi, serves as the internal factor for the onset of the disease. The main pathogenesis involves upper excess and lower deficiency. The upper excess is due to "liver" qi depression and stagnation, "liver" fire, and "liver" wind disturbing upward, with qi rushing to the upper body. The lower deficiency is due to "kidney" yin deficiency and damage, with water failing to nourish wood, causing the "liver" to lose nourishment and leading to excessive "liver" yang. Prolonged illness, with yin impairment affecting yang, further results in deficiency of both yin and yang, manifesting corresponding symptoms and signs. Generally speaking, the early stage of the disease is mostly characterized by excessive "liver" yang, the intermediate stage [second stage] often involves "liver" and "kidney" yin deficiency, and the advanced stage is mostly marked by deficiency of both yin and yang.
bubble_chart Pathological Changes
Small artery lesions are the most important pathological changes in hypertension. In the early stages of hypertension, systemic small arteries spasm. Long-term repeated spasms cause the inner membrane of small arteries to undergo hyaline degeneration due to increased pressure load, ischemia, and hypoxia. The middle layer thickens due to the proliferation and hypertrophy of smooth muscle cells, leading to vascular wall remodeling. Eventually, the vessel wall becomes fibrotic, and the lumen narrows, resulting in irreversible lesions. In rapidly progressive hypertension, small artery walls can develop fibrinoid necrosis within a short period. Small artery lesions at all stages can narrow the lumen, promoting the maintenance and progression of hypertension. The above lesions can occur in small arteries of surrounding tissues and organs, but they are most pronounced in the small arteries of the kidneys. Ultimately, these lesions lead to ischemic injury in tissues and organs.
(1) Heart Left ventricular hypertrophy is the most characteristic change in the heart of hypertensive patients. The primary cause of left ventricular hypertrophy is the long-term narrowing of systemic small artery lumens, which increases peripheral vascular resistance. However, the degree of myocardial hypertrophy does not always correlate positively with the degree of blood pressure elevation. Recent studies have found that catecholamines released during sympathetic stimulation can stimulate myocardial cell protein synthesis. Additionally, Ang II and aldosterone from the RAA system can not only stimulate myocardial cell hypertrophy but also promote the proliferation of collagen scaffolds between myocardial cells, which may also contribute to myocardial hypertrophy in some patients. In the early stages, left ventricular hypertrophy is mainly concentric. Over time, degenerative changes occur in the myocardium, with atrophy of myocardial cells and interstitial fibrosis. The ventricular wall may thin, and the left ventricular cavity may enlarge. During myocardial hypertrophy, coronary blood flow reserve decreases. Combined with the tendency for coronary atherosclerosis in hypertension, myocardial ischemia worsens, exacerbating cardiac lesions. The physiological generation and transformation of the myocardium in hypertension closely resemble changes seen in heart failure, suggesting that myocardial hypertrophy in hypertension may be part of a cardiomyopathy process. Without treatment, it will eventually lead to heart failure. Recent studies have found that certain antihypertensive drugs, particularly ACE inhibitors, may reverse myocardial hypertrophy. The role of local neurohumoral factors and myocardial tissue ACE in myocardial hypertrophy and its reversal is a topic of significant interest.
In elderly patients, due to age-related changes, myocardial cells decrease while collagen tissue increases relatively. Under normal conditions, the heart's systolic and diastolic functions compensate for the physiological loss of myocardium, making myocardial hypertrophy less likely to occur in hypertension. Changes in cardiac function in hypertensive patients may appear before abnormalities are detected in imaging studies.
(2) Central Nervous System Small arteries in the brain can also undergo a series of changes from spasm to sclerosis. However, the structure of cerebral blood vessels is relatively fragile, becoming even more vulnerable after sclerosis. Additionally, long-term hypertension can lead to the formation of microaneurysms in small cerebral arteries, making them prone to rupture and hemorrhage during vascular spasms or fluctuations in intravascular pressure. Small artery ruptures often occur in the internal capsule and basal ganglia. On the basis of small artery sclerosis, thrombosis can form, leading to cerebral infarction. After infarction, softening of brain tissue may cause hemorrhage in the surrounding brain tissue. Hypertension also predisposes to atherosclerosis. If atherosclerosis affects medium-sized cerebral arteries, it can exacerbate cerebral ischemia. Atherosclerotic plaques in intracranial or extracranial arteries can detach, causing cerebral embolism.
(3) Kidney The renal arterioles are the most significantly affected, primarily occurring in the afferent arterioles. The interlobular arterioles may also be involved, but unless combined with diabetes, the efferent arterioles are less frequently affected. The affected blood vessels exhibit narrowed or even occluded lumens, leading to renal cortical ischemia, glomerular fibrosis, tubular atrophy, and interstitial fibrosis, which gradually thins the renal cortex. Relatively normal nephrons may undergo compensatory hypertrophy. In the early stages, the kidneys appear unchanged externally. However, as the disease progresses, the renal surface becomes granular, and the kidney volume may gradually shrink and diminish. These pathological changes are observed in slowly progressive hypertension. Due to the slow progression of the disease, it is termed benign nephrosclerosis, but it ultimately leads to renal failure.
In accelerated hypertension, fibrinoid necrotizing inflammation occurs in the small arteries of the middle layer, and the lesions can directly extend to the glomerular capillary tufts, leading to glomerulosclerosis. In the interlobular and arcuate arteries, there is cellular proliferation in the membrane, with collagen and fibroblasts arranged concentrically in an "onion-skin" pattern. Due to the rapid progression of the disease, patients develop renal failure within a short period, known as malignant nephrosclerosis.
(4) Retina In the initial stage of the disease, the small arteries of the retina undergo spasm, followed by gradual sclerosis. In severe cases, retinal hemorrhage, exudation, and optic disc edema occur. Clinically, changes in the retinal arteries observed through fundoscopy can reflect alterations in other small arteries, particularly those in the brain.
(5) Aorta In the late stage (third stage) of hypertension, cystic medial necrosis and dissection of the aortic wall may occur. The latter is most common at the junction of the aortic arch and descending aorta but can also occur in the ascending aorta, leading to aortic valve insufficiency. In this condition, high-pressure blood tears the aortic intima, allowing large amounts of blood to enter the media, separating the intima and media to form a false lumen. Additionally, hypertension promotes the development and progression of aortic atherosclerosis.
bubble_chart Clinical Manifestations
Hypertension can be divided into two types based on the speed of onset, progression, and duration of the disease: the chronic type and the accelerated type. The former is also known as benign hypertension, and the vast majority of patients fall into this category. The latter is referred to as malignant hypertension, accounting for only 1–5% of hypertensive patients.
(1) Chronic Hypertension This type mostly occurs in middle-aged or older individuals, though those with a family history may develop it at a younger age. The onset is usually insidious, with slow progression and a long course. In the early stages, patients experience fluctuating blood pressure, alternating between high and normal levels—this is known as the brittle hypertension phase. Blood pressure tends to rise during exertion, mental stress, or emotional fluctuations but often returns to normal after rest or removal of these triggers. As the condition progresses, blood pressure gradually increases and becomes more persistent or exhibits smaller fluctuations. The severity of subjective symptoms may not correlate with the degree of blood pressure elevation. About half of the patients show no obvious symptoms and are only diagnosed during routine check-ups or when seeking treatment for other illnesses. A small number of patients are diagnosed only after complications involving the heart, brain, or kidneys occur.
Patients may experience headaches, often localized in the occipital region, particularly upon waking. Other symptoms include dizziness, a sensation of head fullness, neck stiffness, tinnitus, blurred vision, forgetfulness, difficulty concentrating, insomnia, restlessness, fatigue, numbness in the limbs, and palpitations. Not all of these symptoms are directly caused by hypertension; some result from dysfunction of higher social functions and lack clinical specificity. Additionally, recurrent bleeding in different parts of the body may occur, such as subconjunctival hemorrhage, epistaxis, or hypermenorrhea, with a few cases presenting hemoptysis.
In the early stages, patients may experience more symptoms due to significant blood pressure fluctuations. However, after prolonged hypertension, even high blood pressure levels may not cause noticeable symptoms. Therefore, patients should have their blood pressure monitored regularly, regardless of whether symptoms are present. As the disease progresses, blood pressure becomes markedly and persistently elevated, leading to organic damage and functional impairment in the brain, heart, kidneys, and retina, along with corresponding clinical manifestations. When complicated by atherosclerosis, systolic blood pressure elevation is often more pronounced. After myocardial infarction or cerebral hemorrhage, blood pressure may drop to normal levels and remain there long-term or permanently.
1. Neurological Manifestations Headache, dizziness, and head fullness are common neurological symptoms of hypertension. Patients may also experience a heavy sensation in the head or neck stiffness. Hypertension-induced headaches often occur in the morning, localized in the forehead, occiput, or temples, possibly due to dilation of extracranial carotid artery vessels and increased pulse amplitude. These patients typically have very high diastolic pressure, and headaches may improve with antihypertensive treatment. Dizziness caused by hypertension can be transient or persistent; if accompanied by vertigo, it may be related to vascular dysfunction in the inner ear labyrinth and can also improve with medication. However, excessive blood pressure reduction may also induce dizziness.
Hypertensive cerebrovascular diseases are collectively referred to as cerebrovascular accidents, commonly known as apoplexy or apoplexy, and can be divided into two major categories: ①Ischemic infarction, which includes various types such as atherosclerotic thrombosis, lacunar infarction, embolism, transient ischemic attack, and undetermined types. ②Hemorrhage, including parenchymal hemorrhage and subarachnoid hemorrhage. Most cerebrovascular accidents involve only one hemisphere, affecting the contralateral side of the body, while about 15% may occur in the brainstem, affecting both sides. Depending on the type, location, extent, and severity of the cerebrovascular lesion, clinical symptoms vary greatly. Mild cases may present with transient dizziness, vertigo, blindness, aphasia, dysphagia, facial deviation, limb weakness, or even hemiplegia, but these symptoms may gradually recover within minutes to days. Severe cases may suddenly manifest as hemiplegia, facial deviation, vomiting, urinary incontinence, followed by unconsciousness, deep and snoring respiration, unequal pupil size, sluggish or absent reflexes, flaccid paralysis, or pathological signs. Some patients may exhibit increased neck stiffness, while others may only show unconsciousness without focal neurological signs. In critical cases, unconsciousness rapidly worsens, blood pressure drops, and irregular breathing or Cheyne-Stokes respiration may appear, leading to death within hours to days. Patients with less severe unconsciousness may gradually regain consciousness within days to weeks, but some clinical symptoms may not fully recover, leaving varying degrees of sequelae.
Cerebral hemorrhage has a sudden onset, often triggered by emotional agitation, heavy lifting, or straining during bowel movements, leading to a sudden rise in blood pressure and abrupt symptoms, usually with a severe condition. Cerebral infarction also has an acute onset. Cerebral thrombosis develops more gradually, often occurring during rest or sleep, with initial symptoms such as dizziness, limb numbness, or speech impairment, followed by progressive hemiplegia, generally without unconsciousness or only mild unconsciousness (see the chapter on "Acute Cerebrovascular Disease").
2. Cardiac Manifestations Persistent high blood pressure increases the workload of the left ventricle, which compensates by gradually thickening and dilating, leading to hypertensive heart disease.
Recent studies have found that the earliest cardiac effect of hypertension is impaired left ventricular diastolic function. Left ventricular hypertrophy reduces diastolic compliance, affecting relaxation and filling, which may even occur in borderline hypertension or before left ventricular hypertrophy develops. This is likely due to collagen deposition and fibrosis in the myocardial interstitium, though patients may show no obvious clinical symptoms.
Clinically symptomatic hypertensive heart disease typically develops years to decades after the onset of hypertension. During the compensatory phase of cardiac function, symptoms may be minimal except for occasional palpitations. When decompensation occurs, left heart failure symptoms emerge, initially manifesting as panting, palpitations, and coughing during physical exertion, after meals, or excessive talking. These symptoms may later become paroxysmal, often occurring at night, and may include blood-streaked sputum. Severe cases or sudden spikes in blood pressure can lead to cerebral edema. Repeated or sustained left heart failure may impair right ventricular function, progressing to total heart failure with symptoms like oliguria and edema. Before cardiac enlargement, physical examination may reveal only a forceful pulse or apical impulse, or an accentuated second heart sound at the aortic valve area due to elevated aortic diastolic pressure. After cardiac enlargement, examination may show leftward and downward displacement of the cardiac border, a heaving apical impulse, and a grade II-III systolic blowing murmur at the apex and/or aortic valve area. The apical murmur results from left ventricular dilation causing relative mitral regurgitation or papillary muscle dysfunction, while the aortic murmur is due to aortic dilation causing relative aortic stenosis. The second heart sound at the aortic valve may become metallic due to aortic and valve sclerosis, and a fourth heart sound may be present. In heart failure, the heart rate increases, cyanosis appears, a gallop rhythm may be heard at the apex, the second heart sound at the pulmonary valve intensifies, moist rales appear at the lung bases, and pulsus alternans may occur. In the late stage (third stage), symptoms include jugular vein distension, hepatomegaly, lower limb edema, ascites, and worsening cyanosis.
Since hypertension accelerates atherosclerosis, some patients may develop coronary artery disease, presenting with angina or myocardial infarction.
3. Renal Manifestations The severity of renal vascular lesions correlates closely with blood pressure levels and disease duration. Essentially, all uncontrolled hypertensive patients have renal damage, though early stages may lack clinical symptoms. As the disease progresses, nocturia may appear first. Without complications like heart failure or diabetes, 24-hour urinary protein rarely exceeds 1g, and blood pressure control can reduce proteinuria. Hematuria may occur, mostly microscopic, with rare hyaline or granular casts. When renal compensation fails, impaired concentrating ability leads to polyuria, nocturia, thirst, and polydipsia. Urine specific gravity gradually declines, eventually stabilizing around 1.010 (isosthenuria). Further renal decline reduces urine output, with elevated blood non-protein nitrogen, creatinine, and urea nitrogen. Phenolsulfonphthalein excretion decreases markedly, and urea or creatinine clearance rates drop significantly. These changes worsen with renal damage, ultimately leading to uremia. However, in slow-progressing hypertension, most patients die from cardiovascular or cerebrovascular complications before uremia develops.
(2) Accelerated Hypertension Among untreated patients with primary hypertension, approximately 1% may develop accelerated hypertension. The onset can be abrupt or may follow a history of chronic hypertension of varying duration. The male-to-female ratio is about 3:1, and it predominantly occurs in young and middle-aged adults. In recent years, this type of hypertension has become rare, likely due to the early detection of mild grade II hypertension and timely, effective treatment. Its manifestations are largely similar to those of chronic hypertension, but symptoms such as headache are more pronounced, with severe conditions, rapid progression, retinal lesions, and rapid renal failure. Blood pressure is significantly elevated, with diastolic pressure often persistently at 17.3–18.7 kPa (130–140 mmHg) or higher. Various symptoms are evident, and fibrinoid necrosis of small arteries progresses rapidly. Severe damage to the brain, heart, and kidneys often occurs within months to 1–2 years, leading to cerebrovascular accidents, heart failure, and uremia. Blurred vision or blindness is common, with retinal hemorrhages, exudates, and optic disc edema. Plasma renin activity is high. Due to prominent kidney damage, persistent proteinuria is common, with 24-hour urinary protein reaching 3g, along with hematuria and casts. Most patients ultimately die from uremia, though some may succumb to cerebrovascular accidents or heart failure.
（3）Hypertensive Emergencies
1. Hypertensive Crisis During the progression of hypertension, if systemic small arteries undergo temporary intense spasm, leading to a significant increase in peripheral vascular resistance and a sharp rise in blood pressure, accompanied by a series of clinical symptoms, it is termed a hypertensive crisis. This is an acute and severe condition in hypertension, which can occur in any stage of chronic hypertension or in accelerated hypertension. The blood pressure change is primarily characterized by a sudden and marked increase in systolic pressure, though diastolic pressure may also rise. It often occurs under triggering factors such as intense emotional changes, psychological trauma, physical or mental overexertion, cold stimulation, and endocrine disorders (e.g., menstruation or menopause). Patients may experience severe headache, dizziness, vertigo, as well as nausea, vomiting, chest tightness, palpitations, shortness of breath, blurred vision, abdominal pain, frequent urination, oliguria, or dysuria. Some may also exhibit symptoms of autonomic nervous system dysfunction, such as fever, dry mouth, sweating, agitation, flushed or pale complexion, and trembling hands and feet. In severe cases, especially when accompanied by target organ damage, symptoms like angina pectoris, pulmonary edema, renal failure, or hypertensive encephalopathy may occur. During an episode, small amounts of protein and red blood cells (hematuria) may appear in the urine, and levels of blood urea nitrogen, creatinine, epinephrine, and norepinephrine may increase. Blood sugar may also rise. Fundus examination may reveal arterial spasm, possibly accompanied by hemorrhage, exudates, or optic disc edema. The episode is generally short-lived, and the condition may improve rapidly after blood pressure control, though recurrence is common. With the widespread use of effective antihypertensive medications, this crisis has become rare.
2. Hypertensive Encephalopathy In patients with accelerated or severe chronic hypertension, especially those with significant cerebral arteriosclerosis, persistent and marked spasm of cerebral small arteries may occur, followed by passive or forced dilation. Acute cerebral circulatory disturbances lead to cerebral edema and increased intracranial pressure, resulting in a series of clinical manifestations collectively termed hypertensive encephalopathy. The onset is often marked by a sudden rise in blood pressure, with both systolic and diastolic pressures elevated, though the latter predominates. Patients may experience severe headache, dizziness, nausea, vomiting, restlessness, slow but strong pulses, difficulty or slowed breathing, visual disturbances, blackouts, spasms, confusion, or even unconsciousness. Temporary hemiplegia, aphasia, or hemisensory disturbances may also occur. Examination may reveal optic disc edema, increased cerebrospinal fluid pressure, and elevated protein levels. Episodes may last from minutes to hours or even days. Patients with pregnancy-induced hypertension syndrome, glomerulonephritis, renovascular hypertension, or pheochromocytoma may also develop this critical condition.
Stages of Hypertension
Currently, China still follows the revised 1979 clinical staging criteria for hypertension, which divides the condition into three stages based on clinical manifestations:
Stage I (Initial Stage) Blood pressure reaches the diagnostic level for hypertension, with no clinical manifestations of heart, brain, or kidney complications.
Stage II (Intermediate Stage) Blood pressure reaches the diagnostic level for hypertension, accompanied by one of the following: ① Left ventricular hypertrophy detected by physical examination, X-ray, electrocardiogram, or ultrasound; ② Generalized or localized narrowing of retinal arteries on fundus examination; ③ Proteinuria and/or grade I elevation in plasma creatinine concentration.
Stage III (Late Stage) Blood pressure reaches the diagnostic level for hypertension, accompanied by one of the following: ① Cerebrovascular accident or hypertensive encephalopathy; ② Left heart failure; ③ Renal failure; ④ Retinal hemorrhage or exudates, with or without optic disc edema.
Accelerated Hypertension (Malignant Hypertension) The condition progresses rapidly, with diastolic pressure persistently exceeding 17.3 kPa (130 mmHg), accompanied by retinal hemorrhage, exudates, or optic disc edema.
From the above staging, it can be seen that the initial stage [first stage] has no organ injury, the intermediate stage [second stage] already has organ injury, but its function can still be compensated, while the late stage [third stage] has decompensated function of the injured organ.
Hypertension can be classified into grade III based on diastolic blood pressure levels:
grade I: diastolic pressure 12.7～13.9kPa (95～104mmHg)
grade II: diastolic pressure 14.0～15.2kPa (105～114mmHg)
grade III: diastolic pressure ≧15.2kPa (115mmHg)
According to Chinese medicine differentiation, this disease can be divided into three types:
(1) "Liver" yang excess type: Manifested as headache, irritability, insomnia, dry and bitter mouth, red face and eyes, red tip and edges of the tongue, yellow coating, and wiry, forceful pulse.
(2) "Liver" and "kidney" yin deficiency type: Manifested as a sensation of emptiness in the head, headache, vertigo, tinnitus, facial flushing, feverish feeling in palms and soles, weakness in the waist and knees, irritability, palpitation, lack of strength, insomnia, forgetfulness, red and dry tongue, thin coating or scanty coating, and wiry-thin or deep-thin pulse.
(3) Deficiency of both yin and yang type: Manifested as severe vertigo, feeling lightheaded and weak while walking, pale complexion, palpitation and shortness of breath, facial or lower limb edema, frequent nocturia, memory decline, fear of cold, cold limbs, soreness and weakness in the waist and knees, chest tightness, vomiting, or sudden fainting, pale and tender tongue texture, thin white coating or no coating, and deep-tight pulse.
bubble_chart Auxiliary Examination
Laboratory tests can assist in the diagnosis and classification of primary hypertension, assess the functional status of target organs, and aid in the appropriate selection of medications for treatment. Routine tests for hematuria, renal function, uric acid, blood lipids, blood glucose, electrolytes (especially blood potassium), electrocardiogram (ECG), chest X-ray, and fundus examination should be standard for hypertensive patients.
(1) **Blood Routine Test**: Red blood cells and hemoglobin are generally normal. However, in cases of accelerated hypertension, there may be microvascular hemolytic anemia with a negative Coombs test, accompanied by deformed red blood cells. Elevated hemoglobin increases blood viscosity, raising the risk of thrombotic complications (including cerebral infarction) and left ventricular hypertrophy.
(2) **Urine Routine Test**: Early-stage patients typically show normal urine results. As renal concentrating function declines, urine specific gravity gradually decreases, with possible traces of protein, red blood cells, and occasional casts. With disease progression, proteinuria increases. In benign nephrosclerosis, 24-hour urinary protein exceeding 1g indicates a poor prognosis. Red blood cells and casts (mainly hyaline and granular) may also increase.
(3) **Renal Function Test**: Blood urea nitrogen (BUN) and creatinine are commonly used to estimate renal function. Early-stage patients may show no abnormalities, but levels rise once renal parenchymal damage reaches a certain degree. In adults, creatinine >114.3 μmol/L, or >91.5 μmol/L in the elderly and pregnant individuals, suggests renal impairment. Tests such as phenol red excretion, urea clearance, and endogenous creatinine clearance may fall below normal.
(4) **Chest X-ray**: Findings may include elongation and tortuosity of the aorta, particularly in the ascending and arch regions, with possible dilation of the ascending, arch, or descending portions. In hypertensive heart disease, left ventricular enlargement is observed, which becomes more pronounced in left heart failure. In cases of total heart failure, both ventricles may enlarge, accompanied by signs of pulmonary congestion. Pulmonary edema manifests as significant interstitial congestion, appearing as a butterfly-shaped shadow. Routine X-rays are recommended for comparative follow-up.
(5) **Electrocardiogram (ECG)**: Left ventricular hypertrophy may appear as left ventricular enlargement or strain on ECG. Diagnostic criteria vary, but sensitivity and specificity are similar, with false negatives at 68–77% and false positives at 4–6%, indicating moderate sensitivity. Due to reduced left ventricular diastolic compliance and increased left atrial load, ECG may show widened or notched P waves and an increased negative terminal potential of Pv1, sometimes preceding detectable left ventricular hypertrophy. Arrhythmias such as premature ventricular contractions or atrial fibrillation may also occur.
(6) **Echocardiography**: Currently considered the most sensitive and reliable method for diagnosing left ventricular hypertrophy compared to chest X-rays and ECG. Measurements can be taken via M-mode or two-dimensional imaging, with ventricular septum and/or posterior wall thickness >13 mm indicating hypertrophy. Hypertension-related hypertrophy is usually symmetric, but about one-third of cases show predominant septal thickening (septum-to-posterior wall ratio >1.3). Septal thickening often begins superiorly, suggesting early impact on the left ventricular outflow tract. Echocardiography also evaluates cardiac chambers, valves, and aortic root, along with cardiac function. Early-stage hypertrophy may preserve overall function (e.g., cardiac output, ejection fraction) but shows reduced systolic and diastolic compliance, such as decreased maximum contraction rate (Vmax), prolonged isovolumic relaxation, and delayed mitral valve opening. In left heart failure, echocardiography reveals enlarged left ventricle and atrium, with weakened wall motion.
(7) **Fundus Examination**: Central retinal artery pressure may be elevated. The following changes are observed at different stages:
**Grade I**: Retinal artery spasm.
Grade II A: Retinal membrane stirred pulse grade I sclerosis
B: Retinal membrane stirred pulse significantly hardened
Grade III: Grade II plus retinal membrane lesions (hemorrhage or exudation)
Grade IV: Grade III plus optic disc edema
(8) Other examinations: Patients may present with increased serum total cholesterol, triglycerides, low-density lipoprotein cholesterol, decreased high-density lipoprotein cholesterol, and reduced apolipoprotein A-I. Elevated blood glucose and hyperuricemia are also common. Some patients show increased plasma renin activity and elevated angiotensin II levels.
The diagnosis of hypertension should include the following aspects: ① Confirmation of hypertension, i.e., whether the blood pressure is indeed higher than normal; ② Exclusion of symptomatic hypertension; ③ Staging and grading of hypertension; ④ Assessment of the function of vital organs such as the heart, brain, and kidneys; ⑤ Identification of any coexisting conditions that may affect the progression and treatment of hypertension, such as coronary heart disease, diabetes, hyperlipidemia, hyperuricemia, chronic respiratory diseases, etc.
Due to the variability of blood pressure, hypertension should only be diagnosed when elevated blood pressure is measured at least twice on separate occasions under resting conditions. The blood pressure value should be calculated as the average of three consecutive measurements. It is important to note that emotional agitation and physical activity can cause transient increases in blood pressure. When the subject's arm circumference exceeds 35 cm or there is significant stirred pulse atherosclerosis, the blood pressure measured by the cuff method may be higher than the actual blood pressure. In recent years, "white coat hypertension" has attracted attention, where blood pressure readings in a clinical setting are higher than normal due to environmental stimuli, but the individual does not actually have hypertension. The reported incidence of white coat hypertension varies, approximately around 30%. When the diagnosis is in doubt, a cold pressor test can be performed. Hypertensive patients will show an increase in systolic blood pressure of more than 4.7 kPa (35 mmHg) and diastolic blood pressure of more than 3.3 kPa (25 mmHg). To clarify the diagnosis, stirred pulse blood pressure monitoring can also be conducted. This test can observe diurnal blood pressure variations, aiding not only in diagnosis but also in determining the type of hypertension. About 80% of hypertensive patients exhibit a "dipper" pattern in their ambulatory blood pressure curve, where blood pressure is higher during the day and lower at night, with nighttime blood pressure being 10–20% lower than daytime blood pressure. A small proportion of patients have consistently high blood pressure throughout the day and night, showing a "non-dipper" pattern, which may have a greater impact on target organs. Ambulatory blood pressure monitoring provides more comprehensive and detailed information than random blood pressure measurements when assessing the effects and efficacy of antihypertensive drugs. Therefore, it has been increasingly widely used in clinical practice.
For patients who suddenly develop significant hypertension (especially young individuals), those with hypertension accompanied by palpitation, profuse sweating, lack of strength, or other uncommon symptoms of hypertension, those with marked discrepancies in blood pressure between the upper and lower limbs, or those with vascular murmurs in the abdomen or waist, the possibility of secondary hypertension should be considered, and further examinations should be conducted for differentiation. Additionally, attention should be paid to distinguishing it from conditions such as stirred pulse atherosclerosis, hyperkinetic circulatory states, and systolic hypertension caused by increased cardiac output.
All hypertensive patients should undergo routine urine tests, renal function tests, electrocardiography, chest X-rays, echocardiography, and fundus examinations to assess the function of vital organs. These tests not only help estimate the severity of the condition but also provide reference for treatment. For instance, in patients with concurrent heart failure, certain antihypertensive drugs such as diuretics, peripheral vasodilators, and angiotensin-converting enzyme inhibitors can aid in the treatment of heart failure, whereas others like beta-blockers and verapamil may exacerbate heart failure.
bubble_chart Treatment Measures
Once the diagnosis of hypertension is established, treatment should be considered. Hypertension is a chronic sexually transmitted disease, thus requiring long-term, patient, and active treatment. The primary goal is to reduce stirred pulse blood pressure to normal or as close to normal as possible, in order to control and minimize target organ damage related to hypertension, such as in the brain, heart, kidneys, and peripheral blood vessels. Numerous recent clinical controlled trials have shown that lowering blood pressure to normal levels through antihypertensive drugs or non-pharmacological treatments can reduce the incidence and mortality of brain apoplexy in hypertensive patients, prevent and correct malignant hypertension, and lower the fatality rate of main stirred pulse aortic dissection. However, it has not yet been proven that lowering blood pressure can significantly reduce the incidence of coronary heart disease events (such as acute myocardial infarction and sudden cardiac death). The reasons may include starting antihypertensive drug therapy too late or the treatment duration being insufficient to observe such effects. Whether this is related to the adverse effects of certain antihypertensive drugs has also drawn some attention.
The target organ damage in hypertensive patients is closely related to the degree of elevated blood pressure. Therefore, current clinical practice advocates immediate initiation of antihypertensive drug therapy for patients with moderate or grade III hypertension, or those already exhibiting target organ damage.
Grade I hypertensive patients with diastolic blood pressure between 12.0–14.0 kPa (90–105 mmHg) constitute the majority of hypertensive patients, and their blood pressure often fluctuates due to various factors. For such patients, blood pressure should first be rechecked multiple times on different days within four weeks: ① In some patients, diastolic blood pressure may drop below 12.0 kPa (90 mmHg). These patients do not require treatment but should undergo regular blood pressure follow-ups within the following year (every three months). ② If diastolic blood pressure remains between 12.0–12.7 kPa (90–95 mmHg) after four weeks, non-antihypertensive drug therapy (see below) should be administered, and blood pressure should be rechecked within three months. If diastolic pressure remains unchanged after three months and the patient has no other coronary heart disease risk factors, non-pharmacological treatment should be intensified with regular blood pressure follow-ups. If diastolic pressure is between 12.7–13.3 kPa (95–100 mmHg) after four weeks and accompanied by other coronary heart disease risk factors, or if diastolic pressure exceeds 13.3 kPa (100 mmHg), antihypertensive drug therapy should be initiated, with regular follow-ups and dose adjustments based on blood pressure.
Systolic hypertension is just as dangerous as diastolic hypertension. Recent multicenter clinical trial results indicate that with blood pressure control through antihypertensive treatment, the incidence of brain apoplexy, coronary heart disease, and overall mortality are reduced. Therefore, systolic hypertension should also be actively treated, but excessive blood pressure reduction should be avoided in elderly patients with systolic hypertension.
Long-term hypertension can lead to left ventricular hypertrophy. Recent studies have found that left ventricular hypertrophy is an independent risk factor for cardiac death. Certain antihypertensive drugs (such as methyldopa, calcium antagonists, and angiotensin-converting enzyme inhibitors) can reduce the mass and wall thickness of hypertrophied left ventricles, thereby partially reversing left ventricular hypertrophy. However, it remains unclear whether this reversal can reduce heart blood vascular mortality caused by left ventricular hypertrophy. Some recent experimental animal and human studies suggest that certain antihypertensive drugs (e.g., angiotensin-converting enzyme inhibitors) can improve vascular structural and functional abnormalities, as well as insulin resistance associated with hypertension. The clinical significance of these findings still requires further research.
(1) General Treatment Includes: ① Balancing work and rest, maintaining adequate and good sleep, avoiding and relieving tension, and appropriately using sedatives (e.g., diazepam 2.5 mg, orally). Avoid excessive mental and physical exertion. For grade I hypertensive patients, regular physical exercise (such as qigong and tai chi) can help restore normal blood pressure. However, for grade III hypertensive patients or those with grade II or III hypertension who already show signs of target organ damage, competitive sports, especially isometric exercises, should be avoided. ② Reducing sodium intake (<6g of sodium chloride/day) while maintaining sufficient dietary potassium, calcium, and magnesium intake. ③ Controlling weight: For grade I hypertensive patients with obesity, weight loss alone can often normalize blood pressure. For grade III hypertensive patients with obesity, seasonal weight reduction and antihypertensive drug therapy may be combined. ④ Controlling other risk factors for arterial stiffness, such as smoking and elevated blood lipids.
(II) Antihypertensive Drug Therapy In recent years, research and development of antihypertensive drugs have progressed rapidly. The advent of new types of antihypertensive drugs, particularly beta-blockers, calcium antagonists, and angiotensin-converting enzyme inhibitors, has fundamentally transformed the landscape of hypertension treatment. By selecting or combining various antihypertensive drugs based on the characteristics of different patients, blood pressure can now be controlled in the majority of hypertensive patients.
The classification and characteristics of commonly used antihypertensive drugs are shown in the table.
Table: Commonly Used Antihypertensive Drugs
| Category | Antihypertensive Effect Mechanism | Common Preparations and Oral Dosage | Blood Pressure Reduction | Main Side Effects | Indications | Contraindications | Combination Therapy | |
| Di ur etics | Thi azi des , Pa mi des and Chl or thalidone | Initially reduces plasma and extracellular fluid volume, leading to decreased cardiac output, which normalizes after several weeks. Subsequently, sodium ions in the vascular wall may decrease, reducing resistance in precapillary resistance vessels. | Hydrochlorothiazide 25mg, 1–2 times/day; Chlorthalidone 50mg, once/day; Indapamide 2.5–5mg, once/day | Mild, peak effect reached 3–4 weeks after administration | Hypokalemia, elevated blood glucose, hematuria, increased uric acid and cholesterol | Can be used alone for grade I hypertension. More commonly combined with other antihypertensive drugs to enhance efficacy and reduce side effects of sodium and water retention. Particularly suitable for patients with concurrent heart failure or low plasma renin activity. | Hypokalemia, diabetes, hyperuricemia, primary aldosteronism | Often used in combination with other antihypertensive drugs |
| potassium - sparing diuretic | Same as above. Spironolactone directly antagonizes the effects of aldosterone | Same as above | Hyperkalemia, diarrhea, nausea, vomiting, leg cramps, irregular menstruation | Same as above. Spironolactone is also suitable for bilateral adrenal hyperplasia, inoperable adenomas in primary aldosteronism, and patients with persistent hypertension post-surgery | Renal insufficiency | Often used in combination with thiazide diuretics | ||
| Loop di ur etics | Same as thiazides | Furosemide 20-40mg, 1-2 times/day | Diuretic and antihypertensive effects are stronger and faster than other diuretics | Excessive diuresis can lead to hypotension and hypokalemia | Oral useYaodui is effective in controlling "volume-dependent" hypertension with chronic kidney disease and grade III hypertension | Hyperuricemia, primary aldosteronism | Can be combined with other antihypertensive drugs | |
| Ad ren al co rt ic oid an ta gonists | β bl ock ers | Slows heart rate, reduces myocardial contractility, decreases cardiac output and plasma renin activity | Atenolol 25mg, initially 1-2 tablets, 3 times/day, then gradually increased. Metoprolol 25-50mg, 1-2 times/day | Slow, takes effect within 1 to 2 weeks | Bradycardia, heart failure, bronchospasm, nausea, diarrhea, spasm, dizziness, lack of strength, Raynaud's phenomenon, etc. May increase serum triglyceride and cholesterol levels and decrease high-density lipoprotein cholesterol levels. Sudden discontinuation in patients with coronary heart disease may induce colicky pain. | Can be used as the first-line treatment for mild to moderate hypertension, especially in patients with hyperkinetic circulation. | Congestive heart failure, asthma, diabetes, chronic obstructive pulmonary disease, sick sinus syndrome, second- to third-degree atrioventricular block, peripheral vascular disease. | Can be used in combination with diuretics and vasodilators, but should not be used with diltiazem or verapamil. |
| α re cep tor block ers | Blocks the effects of adrenaline, noradrenaline, and sympathetic nerves on blood vessels (blocks both α1and α2receptors), reducing peripheral resistance. Phenoxybenzamine and phentolamine non-selectively block α1and α2adrenergic receptors. Prazosin selectively blocks α1receptors, causing peripheral vasodilation. | Prazosin 0.5mg, 3 times/day, may be increased to 2mg, 3 times/day within two weeks; terazosin 1–10mg/day; phenoxybenzamine 10–30mg, 1–2 times/day; phentolamine 25–50mg, 3 times/day. | Phentolamine has a short duration of action; phenoxybenzamine lasts more than 24 hours; prazosin has a slow onset, reaching peak effect after 4–8 weeks of use. | Headache, dizziness, lack of strength, tachycardia, first-dose hypotension (prazosin). | Phenoxybenzamine is mainly used for treating hypertension in pheochromocytoma. Prazosin and terazosin are suitable for mild to moderate hypertension. | Use with caution in elderly patients. | Prazosin can be used in combination with diuretics and β-blockers. | |
| α , β re cep tor block ers | Blocks α1and β adrenergic receptors. | Labetalol 100–200mg, 3 times/day. | Slowly. | Similar to β-blockers | Effective for all degrees of hypertension | Bronchial asthma, II-III degree atrioventricular block, bradycardia, peripheral vascular disease | Used in combination with diuretics | |
| C e n t r a l n e r v ou | sStimulates the α receptors of the central nervous system, thereby reducing sympathetic nerve outflow, slowing heart rate, decreasing cardiac output, and lowering peripheral vascular resistance. Inhibits renin and aldosterone secretion. Does not reduce renal blood flow | Clonidine hydrochloride 0.075–0.15mg, 3 times/day, may be increased to 0.15–0.30mg per dose; Methyldopa 250mg, 4 times/day, maximum daily dose should not exceed 3g | Blood pressure begins to drop 30 minutes after taking clonidine, with the maximum hypotensive effect occurring in 2–4 hours, lasting 4–24 hours. Reduces both systolic and diastolic blood pressure in different positions. Methyldopa takes effect 2–5 hours after administration, with effects lasting 24 hours | Fatigue, drowsiness, sexual dysfunction, reversible liver damage, lupus-like syndrome (methyldopa), orthostatic hypotension, drowsiness, dry mouth, rebound hypertension after discontinuation (clonidine) | Suitable for moderate to severe hypertension, especially for those with renal insufficiency and elevated plasma renin activity | Clonidine is not recommended for pregnant women, and methyldopa should not be used by those with liver disease | Used in combination with diuretics and vasodilators (e.g., hydralazine, minoxidil, prazosin). Propranolol, guanethidine, bretylium, and tricyclic antidepressants may counteract the hypotensive effect of clonidine and should not be used together | |
| P e r i p h e r al | R a u wo | lBlocks the storage of catecholamines in sympathetic nerve endings, interfering with adrenergic neurotransmission, leading to reduced peripheral vascular resistance, and also has central inhibitory effects | Reserpine 0.25mg, 2–3 times/day | Mild and long-lasting, generally takes one week to take effect, with the lowest levels reached in 2–3 weeks | stuffy nose, bradycardia, excessive stomach acid, diarrhea, lack of strength, drowsiness, edema, etc. Large or long-term use may lead to severe depression and gastrointestinal bleeding | Used alone for grade I hypertension, combined with other antihypertensive drugs for grade III hypertension; especially suitable for patients with rapid heart rate, nervous tension, and high plasma renin activity | Use with caution in patients with ulcer disease or mental depression. Should not be used with monoamine oxidase inhibitors | Can be combined with other antihypertensive drugs (except monoamine oxidase inhibitors) |
| Post gang li on ic sym pa thetic | Depletes norepinephrine stores in nerve terminals, thereby interfering with adrenergic postganglionic nerve terminal transmission, reducing peripheral small artery resistance. Can slow heart rate and decrease cardiac output | Guanethidine sulfate starts at 10mg, 1-2 times/day, gradually increasing to 60mg/day | Rapid action, takes effect within 24-36 hours after administration, effects can last for 3-4 days after discontinuation, significantly reduces sitting and standing blood pressure | Dry mouth, lack of strength, diarrhea, stuffy nose, edema, impotence, orthostatic hypotension, etc. | Suitable for patients with grade III hypertension | Use with caution in patients with coronary heart disease, heart failure, cerebrovascular disease, or reduced renal function. Not suitable for glaucoma patients. Should not be used with monoamine oxidase inhibitors | Combination with diuretics can enhance the effect | |
| Vas
cu
lar
di
lators | Direct vas cular | Directly acts on small artery smooth muscle, causing artery dilation | Hydralazine 10-25mg, 2 times/day; dihydralazine 12.5-25mg, 3 times/day, can be increased to 200mg/day | Peak effect occurs 3-4 hours after administration, lasting for 24 hours | Increased heart rate, lack of strength, headache, nausea, vomiting, diarrhea, peripheral neuritis, etc. Long-term high-dose use (>400mg/d) may cause manifestations of rheumatoid arthritis and systemic lupus erythematosus. | The efficacy is limited when used alone, and it is often combined with other antihypertensive drugs for patients with grade III hypertension and those with renal insufficiency. | Use with caution in patients with tachycardia, coronary heart disease, aortic dissection, and recent cerebral hemorrhage. Contraindicated in the first half of pregnancy. | Can be used in combination with beta-blockers, reserpine, guanethidine, and diuretics. |
| Minoxidil 2.5mg, 4 times/day, increasing the dose every 2-3 days, up to a maximum of 40mg/day. | The effect is significant and long-lasting, with antihypertensive action lasting more than 12 hours after a single dose. | Side effects include sodium and water retention, hypertrichosis, nausea, tachycardia, and angina. | For patients with significantly elevated blood pressure and renal failure. | Same as above. | Can be used in combination with reserpine, beta-blockers, and diuretics. | |||
| Calcium channel blockers | Inhibit calcium influx through calcium channels in the cell membrane of vascular smooth muscle cells, reducing peripheral vascular resistance and lowering blood pressure. | Nifedipine 10-30mg, 3 times/day or sustained-release tablets 30-60mg, once/day; Amlodipine 2.5-10mg, once/day; Felodipine sustained-release tablets 5-10mg, once/day; Lacidipine 2-6mg, once/day; Nitrendipine 10mg, twice/day; Nisoldipine 5mg, once/day; Nicardipine 10-20mg, 3 times/day or sustained-release tablets 40mg, once/day; Nimodipine 20-40mg, 3 times/day; Diltiazem 30-60mg, 3 times/day or sustained-release tablets 90mg, twice/day; Verapamil 40-80mg, 3 times/day or sustained-release tablets 120-240mg, once/day. | Nifedipine takes effect within 30 minutes after oral administration, with an elimination half-life of 2-5 hours. Controlled-release tablets maintain effective plasma concentration for 24 hours. Amlodipine has an elimination half-life of 36 hours. Calcium channel blockers with long half-lives or sustained-release formulations provide 24-hour blood pressure control and satisfactory trough-to-peak ratios (T/P ratio). | Side effects include facial flushing, headache, vertigo, palpitations, gastrointestinal discomfort, and orthostatic hypotension. Diltiazem and verapamil may also inhibit sinoatrial node function and cardiac conduction. | It is mostly satisfactory for controlling blood pressure in mild grade II hypertension. For grade III hypertension patients, it can be combined with other antihypertensive drugs. It is particularly suitable for those with concomitant colicky pain. Diltiazem and verapamil are also suitable for hypertensive patients with atrial arrhythmias. | Contraindicated in pregnant women. Use diltiazem and verapamil with caution in patients with sinus node dysfunction or cardiac conduction block. | Can be used in combination with diuretics and angiotensin-converting enzyme inhibitors. | |
| A n g i o t e n s i n | Inhibits the conversion of angiotensin I to angiotensin II, slows the degradation of vasodilatory bradykinin, and promotes the release of vasodilatory prostaglandins. | Captopril 12.5–25 mg, 3 times/day; enalapril 5–20 mg, 2 times/day; cilazapril 2.5–10 mg, 1 time/day; benazepril 10–30 mg, 1 time/day; perindopril 2–8 mg, 1 time/day. | The antihypertensive effect is well-established. Cilazapril, benazepril, and perindopril have long elimination half-lives and only need to be taken once daily. | <|||||
