Effects of angiotensin-(1-7) on oxidative stress and functional changes of isolated rat hearts induced by ischemia-reperfusion.
- Author:
Xin-xue LIAO
1
;
Rui-xian GUO
;
Hong MA
;
Li-chun WANG
;
Zheng-hua CHEN
;
Chun-tao YANG
;
Jian-qiang FENG
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin I; pharmacology; Animals; Heart; drug effects; physiology; In Vitro Techniques; Male; Myocardial Reperfusion Injury; metabolism; physiopathology; Oxidative Stress; drug effects; Peptide Fragments; pharmacology; Random Allocation; Rats; Rats, Sprague-Dawley; Superoxide Dismutase; metabolism
- From: Journal of Southern Medical University 2008;28(8):1345-1348
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of angiotensin (Ang)-(1-7) on oxidative stress and functional changes in isolated rat hearts with myocardial ischemia-reperfusion (IR) injury.
METHODSIR injury was induced in isolated rat hearts with the Langendorff' apparatus. The left ventricular systolic pressure (LVSP) of the rat heart was measured using a pressure transducer. Malondialdehyde (MDA) level and superoxide dismutase (SOD) activity in the myocardium were detected using commercial kits.
RESULTSMyocardial ischemia (15 min) and reperfusion (30 min) significantly increased myocardial levels of MDA, and reduced the SOD activity and LVSP (P<0.05). Pretreatment with Ang-(1-7) at 1.0 nmol/L 30 min before ischemia obviously inhibited IR-induced MDA increment and lowering of SOD activity and LVSP. Pretreatment of the rats with intraperitoneal injection of 5 mg/kg indomethacin 1 h before isolation of the heart markedly antagonized the effect of Ang-(1-7) on MDA production, SOD activity and LVSP.
CONCLUSIONAngiotensin-(1-7) can inhibit IR injury-induced oxidative stress and decrease in cardiac contractile function in isolated rat hearts. The mechanism underlying the effect of Ang-(1-7) may be associated with increased secretion of prostaglandin.
