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cGMP/PKG 의존성 신호전달기전에 의한 심장보호효과
박경록 고신대학교(의대) 고신대학교 의과대학 학술지 2005 고신대학교 의과대학 학술지 Vol.20 No.1
Backgrounds : The present investigation tested the hypothesis that cGMP-dependent protein kinase (PKG) activates ATP-sensitive K+ (KATP) channels and thus could be associated with the cardioprotective response of ischemic preconditioning. Methods : PKG-induced KATP channel activation and its cardioprotective effects were studied in rabbit ventricular myocytes using patch-clamp techniques and in heart slice model for simulated ischemia and preconditioning. Results : NO donors and PKG activators facilitated KATP channel activity in a concentration-dependent manner, and their effects were suppressed by PKG inhibitors. Exogenous PKG increased KATP channel activity by a phosphorylation-dependent mechanism. Heart slices preconditioned with a single 5-min anoxia followed by 15-min reoxygenation were protected against subsequent 30-min anoxia and 60-min reoxygenation. The beneficial effects of anoxia were almost completely prevented by glibenclamide and PKG inhibitor. Pretreatment with NO donor or PKG activator mimicked anoxic preconditioning. In heart slices pretreated with NO donor or PKG activator, the cardioprotection was blocked by the concomitant presence of glibenclamide or PKG inhibitor. Conclusion : Taken together with the above results showing that the KATP channel acts downstream of the PKG-pathway in the mediating the protective effect, these data indicate that this mechanism, at least in part, contributes to a signaling pathway that induces ischemic preconditioning.
cGMP/PKG 의존성 신호전달기전에 의한 심장보호효과
박경록 고신대학교 의학부 2005 高神大學校 醫學部 論文集 Vol.20 No.1
Backgrounds: The present investigation tested the hypothesis that cGMP-dependent protein kinase (PKG) activates ATP sensitive K+ (KATP) channels and thus could be associated with the cardioprotective response of ischemic preconditioning. Methods: PKG-induced KATP channel activation and its cardioprotective effects were studied in rabbit ventricular myocytes using path-clamp techniques and in hear slice model for simulated ischemia and preconditioning. Results: No donors and PKG activators facilitated KATP channel activity in a concentration dependent manner, and their effects were suppresed by PKG inhibitors. Exogenous PKG increased KATP channel activity by a phosphorylation-dependent machanism. Heart slices preconditioned with a single 5-min anoxia followed by 15-min reoxygenation were protected against subsequent 30-min anoxia and 60-min reoxygenation. The beneficial effects of anoxia were almost completely prevented by blibenclamide and PKG inhibitor. Pretreatment with NO donor or PKG activator mimicked anoxic preconditioning. In heart slices pretreated with NO donor or PKG activator, the cardioprotection was blocked by the concomitant presence of glibenclamide or PKG inhibitor. Conclusion: Taken together with the above results showing that the KATP channel acts downstream of the PKG-pathway in the mediating the protective effect, these data indicate that this mechanism, at least in part, contributes to a signaling pathway that induces ischemic preconditioning.