Vascular effects of angiotensin (1-7) and its contribution to the effect of the cardiovascular drugs

我们在体内研究了血管紧张素肽在人前臂抗药血管中的作用。我们还建立了血管紧张素肽测定系统，并评价了血管紧张素转换酶（ACE）抑制剂对正常血压和高血压患者血浆血管紧张素（1-7）浓度的影响。血管紧张素（1-7）在人类前臂抵抗中没有直接的血管舒张作用。然而，血管紧张素（1-7）可以拮抗血管紧张素II，而去甲肾上腺素不能诱导血管收缩，这表明血管紧张素（1-7）可能是内源性血管紧张素II拮抗剂。血管紧张素（1-7）显著增强缓激素诱导的人类前臂抵抗血管的血管扩张。这种作用被一氧化氮合酶抑制剂L-NMMA所消除，这表明一氧化氮参与了这种相互作用3。血管紧张素（1-7）诱导的缓激肽的血管舒张作用也被单剂量ACE抑制剂所消除。提示血管紧张素（1-7）对缓激素的ACE依赖性作用。血管紧张素（1-7）也能显著减弱血管紧张素i诱导的血管收缩。这些结果提示血管紧张素（1-7）可能是人体内的内源性ACE抑制剂。慢性ACE抑制剂治疗与原发性高血压患者血浆血管紧张素（1-7）水平显著升高相关，但与血浆血管紧张素II水平不降低相关。血管紧张素（1-7）可能有助于维持人类ACE抑制剂的降压作用。

We investigated effects of angiotensin peptide in human forearm resistant vessles in vivo. We also established the assay system of angiotensin peptides and evaluated effects of angiotensin converting enzyme (ACE) inhibitor on plasma concentration of angiotensin (1-7) in normotensive and hypertensive subjects.1. Angiotensin (1-7) had no direct vasodilating effect in human forearm resistant. However, angiotensin (1-7) antagonized angiotensin II but not noradrenaline induced vasoconstriction, which suggested that angiotensin (1-7) might act as an endogenous angiotensin II antagonist.2. Angiotensin (1-7) significantly potentiated bradykinin-induced vasodilatation in human forearm resistant vessels. This effect was abolised by L-NMMA, nitric oxide synthase inhibitor, which suggested the involvement of nitric oxide in this interaction3. Angiotensin (1-7) induced potentiation of the vasodilating effect of bradykinin was also abolished by the single dose of ACE inhibitor., which suggested ACE dependent effect of angiotensin (1-7) on bradykinin. Angiotensin (1-7) also significantly attenuated angiotensin I-induced vasoconstriction. These results suggested that angiotensin (1-7) might be an endogenous ACE inhibitor in man.4. Chronic treatment with ACE inhibitors was associated with significant increased levels of plasma angiotensin (1-7) levels but not decreased levels of plasma angiotensin II in patients with essenstila hypertension. Angiotensin (1-7) may contribute to maintenance of hypotensive effect of ACE inhibitors in man.