Mechanisms of cardioprotection induced by preconditioning after activation of MITOK(ATP) channel.
- Author:
Bei ZHANG
1
;
Bo-yu TANG
;
Hong ZHANG
;
Li ZHU
;
Ying-ying CHEN
;
Yue-liang SHEN
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin-Converting Enzyme Inhibitors; pharmacology; Animals; Cell Membrane; metabolism; Ischemic Preconditioning, Myocardial; methods; Male; Mitochondria, Heart; metabolism; Potassium Channels; metabolism; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2007;23(2):190-193
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo determine mechanisms of cardioprotection induced by combination angiotensin-converting enzyme inhibitors (ACEI) with subthreshold preconditioning after activation of mitochondrial ATP-sensitive potassium (mitoK(ATP)) channel.
METHODSThe Langendorff model of isolated rat heart was used. The time of the onset of uncoupling, the activities of sarcolemmal Na+/K+ -ATPase and Ca2+/Mg2+ -ATPase were measured.
RESULTSThe subthreshold preconditioning (2 min of ischemia and 10 min reperfusion) or captopril (an ACEI) alone did not protect hearts against injury of sustained ischemia. However combination captopril with subthreshold preconditioning increased LVDP. Pretreatment hearts with mitoK(ATP) channel inhibitor 5-HD abolished the protection effect. Combination captopril with subthreshold preconditioning delayed the onset of uncoupling, and enhanced the activities of sarcolemmal Na+/K+ ATPase and Ca2+/Mg2+ -ATPase in ischemia/reperfusion hearts. But 5-HD cancelled these cardioprotection effects.
CONCLUSIONCombination ACEI with subthreshold preconditioning delays the onset of cellular uncoupling induced by acute ischemia, and promotes the stability of sarcolemmal ion channels, in which activation of the mitoK(ATP) channels may be involved.
