Hypertension is a clinical syndrome characterized by the increase of systemic arterial systolic pressure (SBP) and/or diastolic pressure (DBP). It is one of the most common and important cardiovascular diseases in clinic. Pathogenic factors of hypertension: At present, it is believed that the pathogenesis of hypertension is related to the following factors: 1 Neurological factors: Sympathetic nerve plays a leading role in the short-term regulation of hypertension, but it also plays a role in the long-term regulation of blood pressure. The main feature is that the total peripheral resistance increases. What role does sympathetic nerve play in this process? At present, it is considered that sympathetic nerve is involved in the occurrence of essential hypertension, but it may not play an important role in the maintenance of hypertension. At present, it is believed that the causes of increased sympathetic nerve tension are related to the following external factors: ① central ischemic reaction; (2) High-salt diet can inhibit the oppression of hypothalamus by anterior hypothalamus, weaken reflex and increase sympathetic nerve tension; ③ Response to stress stimulus: If you are depressed for a long time, all the responses can act on the vascular motor center, so as to enhance the sympathetic nerve reactivity. The increase of sympathetic nerve tension mainly causes the increase of blood pressure through the following mechanisms: ① exciting heart B 1 receptor to increase cardiac output; ② Stimulating peripheral vascular A receptor increases peripheral vascular resistance; ③ Contraction of renal arterioles, reduction of renal blood flow and activation of RAAS；; ④ Stimulate adrenal medulla to release adrenaline and norepinephrine, and raise blood pressure.

2 humoral factors (1) renin-angiotensin system (RAS): RAS is composed of a series of peptide hormones and their corresponding enzymes, which is very important for regulating blood pressure, water and electrolytes and maintaining the stability of volume environment. Among them, angiotensin II (AngII) plays the most significant role, and it is the strongest hormone among known endogenous pressor substances. Recent studies have found that RAS exists not only in the blood circulation (circulating RAS), but also in some tissues and organs of human body (such as kidney, adrenal gland, heart, blood vessel wall and brain). Further research also confirmed that hyperrenic hypertension is related to the increase of circulating lattice activity in the pathogenesis of hypertension. Normal renin and low renin hypertension are not only related to aldosterone increasing water and sodium storage, but also tissue RAS plays an important role. The fact that angiotensin converting enzyme inhibitor (ACEI) used in clinic in recent years is effective not only for high renin type, but also for low renin type hypertension also confirms the above theory. Of course, the relationship between circulating RAS and tissue RAS is quite complicated, and their role in the pathogenesis of hypertension is still unclear, which needs further study in the future.

(2) Insulin resistance: Insulin resistance refers to a phenomenon that the biological effect caused by normal concentration of insulin in blood circulation in the body is lower than normal, and there are many reasons that can cause insulin resistance. Including pre-receptor defects (such as insulin resistance in incomplete blood circulation when the molecular structure of insulin is abnormal), receptor level defects (such as the decrease of the number of insulin receptors and the decrease of receptor affinity) and post-receptor defects (such as obesity, diabetes, uremia, etc.). In recent years, it has been found that patients with hypertension (especially essential hypertension) generally have insulin resistance, and insulin resistance exists when blood pressure continues to rise or early hypertension. The fasting insulin level of patients with borderline hypertension is also significantly higher than that of those with normal blood pressure, so it is inferred that insulin resistance has a certain relationship with hypertension, but the exact mechanism is not clear.

(3) Atrial natriuretic peptide (ANP): ANP is a polypeptide hormone synthesized, stored and secreted by atrial myocytes, which has powerful diuretic, vasodilator, antihypertensive, anti-RAS and anti-vasopressin effects. Hypertension patients are often accompanied by decreased ANP response, which may be related to the down-regulation of ANP receptors after long-term stimulation of ANP release by hypertension (the number of ANP receptors decreases and the affinity for ANP decreases).

(4) Endothelin (ET):ET is a vasoactive polypeptide synthesized by vascular endothelial cells, which has a wide range of regulatory effects on cardiovascular, pulmonary, renal endocrine and nervous system functions. ET can cause strong and lasting contraction of arterial veins and microvessels, which is independent of the existence of endothelial cells and is not affected by A and P receptor blockers, but can be reversed by isoprenaline nitroglycerin. ET can also enhance myocardial contractility; Reducing renal blood flow by contracting renal artery and activating RAAS is the main cause of hypertension.

(5) Vasopressin (VP): VP is a neuropeptide secreted by neurons in supraoptic nucleus and paraventricular nucleus of hypothalamus, which is also called antidiuretic hormone because of its antidiuretic effect. In addition, VP also plays a certain role in maintaining the steady state of normal blood pressure and vascular tension. Recent studies show that VP regulates hypertension (especially essential hypertension) mainly by acting on cardiovascular exercise center, and patients often have an increase in plasma VP concentration.

Function of vascular endothelial cells Vascular endothelial cells play an important role in regulating vascular tension and platelet function. Endothelial cells can produce some vascular relaxing factor, such as prostacyclin (PGI2), endothelial relaxing factor (EDRF), and some contraction factors, such as thromboxane A2(TXA2) mentioned above. Under physiological conditions, the two factors interact with each other, but relaxing factor is slightly dominant, thus inhibiting excessive vasoconstriction and platelet activation and protecting circulation. In aging or some diseases, the role of contraction factor is enhanced (the release of contraction factor is increased, and the responsiveness of blood vessels to contraction factor is also enhanced), which leads to the increase of peripheral vascular resistance and hypertension, mainly the increase of diastolic blood pressure.

The results of epidemiological investigation of genetic factors show that 59% patients with essential hypertension have family history; The blood pressure level of identical twins is closer than that of identical twins. There is no correlation between the blood pressure of adopted children and their adoptive parents and fraternal siblings; The prevalence rate of hypertension in children of parents with normal blood pressure is 3. 1%, and that in children of parents with hypertension is 28.3%. The prevalence rate of children with hypertension in both parents can reach 45.5%; Therefore, genetic factors play an important role in the pathogenesis of hypertension. However, the specific genetic mode and law have not yet been determined. Most scholars believe that essential hypertension is the result of genetic susceptibility and environmental effects, that is, the genetic quality of hypertension is a necessary condition for hypertension. According to the current research on the genetic defects of hypertension, the main manifestations are the defect of cation (Na+K+Ca2+) transport in cell membrane, the defect of sympathetic nerve and its mediator metabolism, the defect of kidney and its secretion related factors, and the genetic defect of platelets.

Others, such as proto-oncogene: the expression of myocardial and vascular wall thickening in people with immune dysfunction, oral contraceptives (increasing blood volume in elderly people with arteriosclerosis (which can cause isolated systolic hypertension) by activating RAAS), etc.

In short, the occurrence of hypertension is a very complicated process. It involves many aspects such as genetic defects in the function of neurohumoral endothelial cells. There are three ways to increase blood pressure: ① the increase of peripheral blood vessels (resistive vasoconstriction)-causing hypertension with diastolic blood pressure increasing; (2) Increased cardiac output (increased heart rate, enhanced myocardial contractility)-hypertension causing increased systolic blood pressure; ③ Increased blood volume or blood viscosity.