A large number of experimental, clinical and epidemiological data confirmed that sodium replacement is closely related to hypertension. In areas with high salt intake, such as native Japanese, the prevalence of hypertension is high, while in areas with low salt intake, such as Eskimos in Alaska, hypertension almost does not occur. Limiting sodium intake can improve hypertension, and taking diuretics to increase sodium excretion can also reduce elevated blood pressure. Renovascular hypertension worsens under the influence of high blood sodium, and improves when the sodium intake is reduced. The application of Desoxycorticosterone can cause hypertension only in the case of salt. The hypertension caused by adrenal hyperplasia also needs the participation of sodium. The contents of sodium and water per unit volume of dry matter in renal artery of patients and animals died of hypertension were higher than those without hypertension. Sodium retention can increase extracellular fluid volume and cardiac output, increase water content of arteriole wall and increase peripheral resistance, and increase arteriole tension due to the change of ratio of intracellular and extracellular sodium concentration. However, laboratory and clinical studies have found that changing the salt intake and blood sodium level can only affect the blood pressure level of some individuals, but not all individuals. Therefore, it is considered that the pathogenesis of salt in diet is conditional, and it has the effect of causing high blood pressure only when there is a genetic defect of sodium movement in the body, which makes it sensitive to salt intake.
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