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Ischemia/reperfusion (I/R) has been associated with ventricular (LV) remodeling, including induction of hypertrophy. Stimulation of α1-Adrenoceptors (ARs) has been implicated in the pathogenesis of cardiac hypertrophy. The present study is to test the hypothesis that α1-AR-mediated hypertrophy is selectively mediated via the oxidative modification of Gh during hypoxia/reoxygenation (H/R) or I/R. Reactive oxygen species (ROS) was increased in H/R and expression level of membrane Gh. To further address involvement of Gh in hypertrophic response, specific relation of Gh was confirmed by using Gh overexpression and blocking into cardiomyocytes. Mainly increased membrane Gh protein by ROS has a more sensitive effect on myocardial hypertrophy through MEK1,2/ERKs signal transduction pathway, but induction of proto-oncogene except c-fos and expression of PLC δ1 was independent in ROS condition. These results provide that ROS production by I/R mediates Gh protein increment and Gh protein leads to more specific responsiveness to NE-stimulated hypertrophic cardiomyocytes.