Pulsatile stretch induces release of angiotensin II and oxidative stress in human endothelial cells:: Effects of ACE inhibition and AT1 receptor antagonism

被引：27

作者：

Gatti, Chiara Delli ^{[1
]}

Osto, Elena ^{[1
]}

Kouroedov, Alexei ^{[1
]}

Eto, Masato ^{[1
]}

Shaw, Sidney ^{[2
]}

Volpe, Massimo ^{[3
,4
]}

Luescher, Thomas F. ^{[1
]}

Cosentino, Francesco ^{[1
,3
]}

机构：

[1] Univ Hosp & Cardiovasc Res, Ctr Cardiovasc, Inst Physiol, Zurich, Switzerland

[2] Univ Bern, Dept Clin Res, CH-3012 Bern, Switzerland

[3] Univ Roma La Sapienza, Fac 2, Rome, Italy

[4] IRCCS Neruomed, Pozzilli, IS, Italy

来源：

CLINICAL AND EXPERIMENTAL HYPERTENSION | 2008年 / 30卷 / 07期

基金：

新加坡国家研究基金会;

关键词：

nitric oxide; free radicals; endothelium; renin angiotensin system;

D O I：

10.1080/10641960802443183

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Mechanical forces and the activation of the renin-angiotensin system (RAS) may alter the NO/O-2(center dot-) balance, imparing endothelial nitric oxide (NO) availability. This study investigates the link between RAS and NO/O-2(center dot-) balance in human aortic endothelial cells (HAEC) exposed to pulsatile stretch with and without ACE inhibitor quinaprilat or angiotensin II type 1 (AT(1)) receptor antagonist losartan. Pulsatile stretch increased Ang II levels and O-2(center dot-) production, reducing NO release. RAS blockade with quinaprilat or losartan restored the balance between NO and O-2(center dot-). These results provide a molecular basis for understanding the vascular protective effects of ACE inhibition and AT(1) receptor antagonism.

引用

页码：616 / 627

页数：12

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