Ferrario C M, Chappell M C, Dean R H, Iyer S N
The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1032, USA.
J Am Soc Nephrol. 1998 Sep;9(9):1716-22. doi: 10.1681/ASN.V991716.
Accumulating evidence suggests that angiotensin-(1-7) is an important component of the renin-angiotensin system, having actions that are either identical to or opposite that of angiotensin II. Angiotensin I can be directly converted to angiotensin-(1-7), bypassing formation of angiotensin II. This pathway is under the control of three enzymes: neutral endopeptidases 24.11 (neprilysin) and 24.15 and prolyl-endopeptidase 24.26. Two of the three angiotensin-forming enzymes (neprilysin and endopeptidase 24.15) also contribute to the breakdown of bradykinin and the atrial natriuretic peptide. Furthermore, angiotensin-(1-7) is a major substrate for angiotensin-converting enzyme. These observations suggest that the process of biotransformation between the various Ang peptides of the renin-angiotensin system and other vasodepressor peptides are intertwined through this enzymatic pathway. Substantial evidence suggests that angiotensin-(1-7) stimulates the synthesis and release of vasodilator prostaglandins, and nitric oxide, while also augmenting the metabolic actions of bradykinin. In addition, angiotensin-(1-7) alters tubular sodium and bicarbonate reabsorption, decreases Na+-K+-ATPase activity, induces diuresis, and exerts a vasodilator effect. These physiologic effects of angiotensin-(1-7) favor a blood pressure-lowering effect. The majority of the data currently available suggest that angiotensin-(1-7) mediates its effects through a novel non-AT1/AT2 receptor subtype.
越来越多的证据表明，血管紧张素 -（1 - 7）是肾素 - 血管紧张素系统的一个重要组成部分，其作用与血管紧张素II相同或相反。血管紧张素I可以直接转化为血管紧张素 -（1 - 7），而不经过血管紧张素II的形成过程。这条途径受三种酶的控制：中性内肽酶24.11（中性肽链内切酶）、24.15和脯氨酰内肽酶24.26。三种血管紧张素生成酶中的两种（中性肽链内切酶和内肽酶24.15）也参与缓激肽和心房利钠肽的降解。此外，血管紧张素 -（1 - 7）是血管紧张素转换酶的主要底物。这些观察结果表明，肾素 - 血管紧张素系统的各种血管紧张素肽与其他血管舒张肽之间的生物转化过程通过这条酶促途径相互交织。大量证据表明，血管紧张素 -（1 - 7）刺激血管舒张前列腺素和一氧化氮的合成与释放，同时也增强缓激肽的代谢作用。此外，血管紧张素 -（1 - 7）改变肾小管钠和碳酸氢盐的重吸收，降低钠钾ATP酶活性，诱导利尿，并发挥血管舒张作用。血管紧张素 -（1 - 7）的这些生理效应有利于降低血压。目前可得的大多数数据表明，血管紧张素 -（1 - 7）通过一种新型的非AT1/AT2受体亚型介导其作用。
