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口服有效的转化酶抑制剂(CEI)如巯甲丙脯酸或MK 421等,业已成功地作为抗高血压药进入临床。最初认为,CEI的降压机制在于抑制转化酶使循环的血管紧张素Ⅱ(ANG Ⅱ)减少,从而减弱ANG Ⅱ的直接升压作用。然而有证据表明,在高血压病人和实验性高血压动物,不论血浆中肾素-血管紧张素系统是否兴奋,CEI均有降压作用。由于转化酶也是缓激肽的主要降解酶,故CEI亦能增加外原性缓激肽的血管扩张作用。此外,尚有些与转化酶抑制无关的作用,如血管平滑肌对钠通
Oral and potent inhibitors of invertase (CEI), such as captopril or MK 421, have been successfully introduced into the clinic as antihypertensives. It was initially thought that the mechanism of antihypertensive effect of CEI is to inhibit the invertase to reduce the circulating angiotensin II (ANG II), thereby reducing the direct step-up effect of ANG II. However, there is evidence that in hypertensive patients and experimental hypertensive animals, CEI has antihypertensive effects regardless of whether the plasma renin-angiotensin system is excited. Because invertase is also a major enzyme in bradykinin, CEI can also increase the vasodilator effect of exogenous bradykinin. In addition, there are some and invertase inhibition unrelated effects, such as vascular smooth muscle sodium