Role of Angiotensin (1-7) in therapeutic application of inhibition of rennin-angiotensin system in man

1.血管紧张素（1-7）与缓激肽及其他血管活性肽在体内抵抗血管中的相互作用血管紧张素（1-7）可能通过NO系统以剂量依赖的方式显著增强了缓激肽的血管舒张作用。这一结果与先前在离体血管中的研究结果完全一致。2 . NO箝位技术在人体NO研究中的验证我们评估了NO阻尼技术在L-NMMA抑制NO研究中的有效性和可行性。血管紧张素（1-7）在体外和体内的抗氧化作用研究表明，血管紧张素II可能通过增加人体抗氧化血管中超氧化物的产生而减弱NO供体的血管舒张作用。同时输注血管紧张素（1-7）可拮抗该效应，且呈剂量依赖性。在培养的人THP-1细胞中，血管紧张素（1-7）也被发现可以抑制血管紧张素II增加的氧化应激。接受ACE抑制剂治疗的高血压患者血管紧张素（1-7）水平升高单剂量卡托普利可显著提高高血压患者和正常人血浆血管紧张素-(1-7)水平。血浆血管紧张素-(1-7)水平的变化与血压有高度显著的相关性。长期接受ACE抑制剂治疗的高血压患者血浆血管紧张素-(1-7)水平显著高于未接受AGE抑制剂治疗的高血压患者，而血浆血管紧张素II水平差异无统计学意义。急性或慢性ACE抑制剂治疗与血浆血管紧张素-水平升高相关（1-7），这可能有助于ACF抑制的作用。

1.Interaction of Angiotensin(1-7) with bradykin and other vasoactive peptides in human resistant vessels in vivoAngiotensin(1-7) significantly potentiated vasodilating effect of bradykinin in dose-dependent manner possibly through NO system. This result is completely consistent with previous results from studies in isolated vessels.2.Validation of NO clamp technique in human NO research in vivoWe evaluated validity and feasibility of NO damp technique for NO research using L-NMMA for NOS inhibition.3.Anticoxidant effect of Angiotensin(1-7) in vitro and in vivoWe showed Angiotensin II attenuated vasodilating effect of a NO donor possibly through increased production of superoxide in human resisitant vessels. This effect was antagonized by co-infusion of Angiotensin(1-7) in dose dedpendent manner. Angiotensin(1-7) was also found to inhibit increased oxidative stress by Angiotensin II in cultured human THP-1 cells.4.Increased Angiotensin(1-7) levels in patients with hypertension receiving ACE inhibitors. The single dose of captopril significantly elevated plasma levels of angiotensin-(1-7) in hypertensives and normal volunteers. There was highly significant correlation between changes in plasma levels of angiotensin-(1-7) and blood pressure. Plasma angiotensin-(1-7) levels in hypertensive patients chronically receiving ACE inhibitors were significantly higher than those without AGE inhibitors while there was no significant difference in plasma Angiotensin II levels. Either acute or chronic treatment with ACE inhibitors was associated with increased plasma levels of angiotennsin-(1-7), which may contribute to effects of ACF inhibitions.