高血压病因和发病机制英,汉版

on the mechanism of hypertension

The precise mechanisms by which blood pressure is elevated in essential and secondary hypertension remain unknown. The pathophysiology of hypertension involves alterations in the balance between peripheral resistance (PR) and cardiac output (CO). In normal individuals, changes in PR and CO tend to compensate for each other so that mean arterial pressure (MAP) remains relatively constant. However, in patients with hypertension, this equilibrium point shifts upward on the MAP response curve. This shift results from an increase in total peripheral resistance (TPR), primarily due to increased vascular smooth muscle tone and decreased compliance of large elastic arteries.

In primary or essential hypertension, the etiologic factors responsible for the rise in TPR are not known. It has been proposed that hypertension develops as a result of an imbalance between sympathetic nervous system activation and insulin sensitivity. Increased sympathetic activity leads to vasoconstriction and enhanced release of norepinephrine at synapses within the adventitia of small muscular arteries. Norepinephrine binds to receptors on the endothelium, leading to vasodilation. Loss of insulin sensitivity causes an increase in lipolysis and secretion of fatty acids into the circulation. These fatty acids activate the peroxisome proliferator-activated receptor gamma (PPARgamma) and stimulate the production of proinflammatory cytokines. PPARg also stimulates the expression of the transcription factor nuclear peroxisome proliferator-activated receptor alpha (PPARalpha). PPARa regulates the transcription of several genes involved in the regulation of TPR, including those encoding the

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