Effect of calcium channel blocker on gap junctional connexin 43 in infarcted myocardium in rats

AIM:To investigate the effect of cardiac L- and L/T-type Ca2+ channels on gap junctional connexin 43 (Cx43) in myocardium infarcted heart remodeling of rats. METHODS: Rat myocardium infarction model was established by permanent ligation of the left coronary artery. Infarcted rats were treated with oral placebo, amlodipine ［L-channel blockade, 4 mg/(kg·day)］ or mibefradil ［L/T-channel blockade, 10 mg/(kg·day］ beginning 7 days before induction of myocardial infarction (MI). Protein levels of Cx43 were measured 1, 3 and 7 days postcoronary occlusion in the noninfarcted and infarcted myocardium. Infarct size and left ventricular dilation were determined in picrosirius red-stained hearts. RESULTS: MI induced an upregulation of Cx43 protein in the hypertrophied interventricular septum (IS) (maximum 7 days postinfarction), whereas Cx43 protein expression of Cx43 decreased markedly in the infarcted myocardium of left ventricular free wall (LVFW) 1, 3 and 7 days postinfarction, with significant differences compared with those in control group (P<0.01). Carvedilol inhibited the protein upregulation of Cx43 and thickness of IS, decreased left ventricular dilation and reduced infarct size more obviously 7 days postinfarction. CONCLUSIONS: Infarction-induced cardiac hypertrophy is accompanied by upregulation of Cx43 in IS, whereas Cx43 is downregulated in LVFW in the process of cardiac infarcted pathogenesis. Cardiac L- and L/T-type Ca2+ channel blockade differentially reduced postinfarction remodeling, which is associated with the selective regulation of cardiac Cx43 in remodeling myocardium.