Corvol P, Elkik F, Thibonnier M, Plouin P F, Menard J
Nouv Presse Med. 1981 Apr 30;10(19):1525-30.
The recent development of several inhibitors of the renin-angiotensin system has perfected our knowledge of the part played by this system in the control of physiological and pathological arterial pressure. Peptides inhibiting angiotensin II, such as Sar1, Ala8 angiotensin II, block the peripheral effects of angiotensin on vascular renal and adrenal receptors. Inhibition of the conversion enzyme, notably with captopril, prevents the formation of angiotensin II from angiotensin I and also results in accumulation of a vasodilator and natriuretic peptide: bradykinin. Finally, it is now possible to inhibit more specifically the reaction of renin with its substrate, angiotensinogen, by using pepstatin or its derivatives, or peptide analogues of the substrate. The use of these inhibitors, especially captopril (so far the most studied), has made it clear that renin plays a part in experimental and human essential hypertension and participates in the control of arterial blood pressure in subjects with normal sodium intake.
肾素-血管紧张素系统几种抑制剂的最新进展,使我们对该系统在生理和病理动脉血压控制中所起的作用有了更完善的认识。抑制血管紧张素II的肽类,如Sar1、Ala8血管紧张素II,可阻断血管紧张素对血管、肾脏和肾上腺受体的外周作用。特别是用卡托普利抑制转化酶,可阻止血管紧张素I转化为血管紧张素II,还会导致一种血管舒张和利钠肽:缓激肽的蓄积。最后,现在可以通过使用胃蛋白酶抑制剂或其衍生物,或底物的肽类似物,更特异性地抑制肾素与其底物血管紧张素原的反应。这些抑制剂的使用,尤其是卡托普利(迄今为止研究最多),已明确肾素在实验性和人类原发性高血压中起作用,并参与正常钠摄入受试者的动脉血压控制。