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

1.血管紧张素(1-7)与人在体阻力血管中的缓激肽及其他血管活性多肽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缓激肽的血管扩张作用。2.NO钳技术在体内NO研究中的有效性我们评价了NO阻滞法用于NO研究的有效性和可行性。3.血管紧张素(1-7)的体外和活体抗氧化作用我们证明了血管紧张素II抑制NO供体的血管扩张作用可能是通过增加人体阻力血管中超氧化物的产生。此作用可被血管紧张素(1-7)以剂量依赖的方式联合给药拮抗。血管紧张素(1-7)还可以抑制血管紧张素II增加的人THP-1细胞的氧化应激。4.接受血管紧张素转换酶抑制剂治疗的高血压患者血管紧张素(1-7)水平升高。单剂量卡托普利显著提高高血压患者和正常志愿者的血浆血管紧张素-(1-7)水平。血浆血管紧张素-(1-7)水平变化与血压呈高度正相关。长期服用血管紧张素转换酶抑制剂的高血压患者血浆血管紧张素-(1-7)水平显着高于未服用AGE抑制剂的患者，而血浆血管紧张素II水平无明显差异。血管紧张素转换酶抑制剂的急性或慢性治疗与血浆血管紧张素-(1-7)水平升高有关，这可能与ACF抑制作用有关。

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.