Protective effect of calcium channel blocker on hypertensive rat myocardial remodeling of pressure overload induced by endoplasmic reticulum stress

AIM:To investigate the influence of calcium channel blocker lacidipine on the expression of calreticulin (CRT) and caspase-12 in rat cardiac myocytes and the effects of lacidipine against myocardium remodeling under pressure overload conditions. METHODS: Thirty male Sprague Dawley rats were randomly divided into TAC group (transverse aortic constriction), control group (sham group) and TAC+lacidipine group with ten rats in each group. Invasive hemodynamics were measured through carotid cannulation and left ventricular morphology was monitored by echocardiography. Expressions of CRT and caspase-12 in rat cardiac myocytes were examined by immunohistochemistry, and cardiac myocyte apoptosis was detected by TUNEL fluorescent staining. RESULTS: Compared with those in control group, MAP (mean arterial pressure), IVST (interventricular septal thickness), LVPWT (left ventricular posterior wall thickness), LVWI (left ventricular weight index), expressions of CRT and caspase-12 in cardiac myocytes, and incidence of cardiac myocyte apoptosis remarkably increased in TAC group (P<0.01). Compared with those in TAC group, MAP, IVST, LVPWT, LVWI and incidence of cardiac myocyte apoptosis in TAC+lacidipine group decreased significantly, whereas expressions of CRT and caspase-12 in cardiac myocytes were significantly downregulated (P<0.05). CONCLUSION: The endoplasmic reticulum stress may be involved in the process of myocardium remodeling caused by pressure overload induced-hypertension. Lacidipine may exert a protective effect on the heart by ameliorating the endoplasmic reticulum stress via downregulating the expression of CRT and caspase-12 and decreasing the incidence of cardiac myocyte apoptosis.