Type H hypertension is primary hypertension accompanied by hyperhomocysteinemia (homocysteine, Hcy ≥10umol/L). In a six-city study (Beijing, Shanghai, Nanjing, Shenyang, Harbin, Xi'an), Prof. Li Jianping and others at Peking University First Hospital showed that H-type hypertension accounted for about 75% of adult hypertensive patients in China (91% of men and 60% of women). Hypertension is categorized into primary and secondary. Primary hypertension, also known as hypertensive disease, accounts for more than 90% of hypertensive patients, with some special types of hypertension, such as salt-sensitive hypertension, white coat hypertension, and H-type hypertension. Secondary hypertension has an etiology and is a clinical manifestation of certain diseases, most commonly renal hypertension due to kidney disease. The World Health Organization's CDC Classification of Disease Controls considers the average level of fasting plasma cysteine in healthy adults to be 5-15 umm/L, and when the HCY level is ≥10 umm/L, it is considered to be hyper-HCYemia, and hypertension accompanied by hyper-HCY is referred to as "H-type hypertension".

Main causes

Genetic factors, diet, mental stress, obesity, etc.

English name

homocysteine

Department of medicine

Internal medicine, cardiovascular medicine, etc.

Infectiousness

None

Alternative name

H-type hypertension.

Abbreviation

Hypertension

Causes

Causes of primary hypertension include (1) genetic factors, (2) diet, high sodium and low potassium diets, (3) mental stress, prolonged exposure to tension and high pressure, (4) obesity, and (5) oral contraceptives.

The main reasons for the elevation of Hcy are: (1) insufficient intake of vitamins B6, B12 and folic acid, especially folic acid intake resulting in homocysteine biosynthesis of methionine cycling disorders are closely related; (2) related to the genetic inheritance of the genes, research has confirmed that the homocysteine level of the MTHFRC677TTT genotype is twice as much as that of the CT/CC genotype; (3) a diet rich in methionine protein is not enough to prevent the development of the disease. 3) methionine-rich protein diet.

Mechanism of occurrence

Hyperhomocysteinemia, which is characterized by increased blood Hcy levels, is an independent risk factor for atherosclerosis and arteriosclerosis, and is closely related to peripheral vascular disease and cerebrovascular disease, hypertension and hypertensive heart disease, and coronary artery obstruction and thrombosis. Many studies have found that Hcy can damage vascular endothelial cells and trigger changes in vascular structure, leading to vascular dysfunction. 2010 American scholars conducted a review of studies on the mechanism: hyperhomocysteinemia causes vascular dysfunction mainly through two pathways: the first is to raise blood pressure; the second is to damage the endothelial NO-derived vasodilatory activity. Hcy activates metalloproteinases and induces collagen synthesis leading to elasticity. Hcy activates metalloproteinases, which induce collagen synthesis leading to an imbalance in the elastic-to-collagen ratio and impairing vascular elasticity. Metabolites of high Hcy in the endothelium affect smooth muscle cells, leading to vascular dysfunction and causing hypertension; Hcy is metabolized in vivo to produce hydrogen sulfide (H2S), which is a strong antioxidant and vasodilator. When hyperHcymia, it causes a decrease in H2S production by inhibiting cystathionine-gamma-synthase (CSE), which leads to hypertension and vascular diseases.

Also, the doctrine that hyperhomocysteinemia causes hypertension is associated with increased angiotensin-converting enzyme activity. Some studies have shown that H2S blocks angiotensin-converting enzyme (ACE) activity in endothelial cells. It has also been shown that Hcy induces AT1 receptor-associated metalloproteinase-9 and collagen synthesis in vascular endothelial cells, leading to the development of hypertensive vascular remodeling.