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如何在有效降压的同时保护肾功能是肾性高血压治疗的关键。要做到这一点,就必须根据肾性高血压中肾实质性和肾血管性高血压不同的病理生理背景和不同的病期特点,来选择和调整抗高血压药物。巯甲丙脯酸是1977年合成的非肽类血管紧张素转换酶(ACE)抑制剂,其药理作用基础是以巯基与血管紧张素Ⅰ(ATI)竞争结合含锌的ACE,通过下列途径产生降压效应:(1)减少AT-Ⅱ,降低AT-Ⅱ的全身加压作用,并直接影响AT-Ⅱ的局部组织效应,(2)抑制激肽酶Ⅱ(即ACE),保持激肽活性、(3)增加前列腺素E_2合成,(4)刺激肾髓质脂质分泌。巯甲丙脯酸在肾实质性高血压中的应用:肾实质性高血压的主要发病机理可归纳为七个方面,①容量机制;③肾素机制;③容量及肾素间的异常关联;④前列腺素及其它扩血管物质的减少;⑤交感神经系统的兴奋性增强;⑥利钠因子的机制;⑦具强力缩血管作用的内源性洋地黄物质(EDLS)水平升高及其它激素的影响。在各种肾实质疾患及肾功能不全的不同时期,这些机制都不同程度地参与了高血压的发生与维持。
How to effectively reduce blood pressure while protecting renal function is the key to the treatment of renal hypertension. To do this, we must select and adjust the antihypertensive drugs according to the different pathophysiological background and different stages of renal parenchymal and renovascular hypertension in renal hypertension. Captopril is a non-peptide angiotensin-converting enzyme (ACE) inhibitor synthesized in 1977 and its pharmacological action is based on the competition of sulfhydryl with angiotensin I (ATI) for binding of zinc-containing ACE by the following routes Antihypertensive effects: (1) AT-II is reduced, systemic pressure of AT-II is reduced, and local tissue effects of AT-II are directly affected. (2) Inhibition of kininogen II (ie, ACE) , (3) increase prostaglandin E_2 synthesis, (4) stimulate medullary lipid secretion. The application of captopril in renal parenchymal hypertension: The main pathogenesis of renal parenchymal hypertension can be summarized in seven aspects, ① capacity mechanism; ③ renin mechanism; ③ capacity and abnormal association between renin; ④ reduction of prostaglandins and other vasodilators; ⑤ increased excitability of the sympathetic nervous system; ⑥ mechanisms of natriuretic factor; and ⑦ elevated levels of endogenous digitalis (EDLS) with potent vasoconstrictor and other hormones influences. In a variety of renal parenchymal disorders and renal dysfunction in different periods, these mechanisms are involved to varying degrees, the occurrence and maintenance of hypertension.