Effects of telmisartan on angiotensin II-induced cardiomyocyte hypertrophy and p-ERK1/2 phosphorylation in rat cultured cardiomyocytes

Abstract

Background: Cardiomyocyte hypertrophy is a common complication of hypertension, and is recognized as an important risk factor for cardiovascular diseases. Up to now, no study has been made on the effects of telmisartan on Ang II-induced cardiomyocyte hypertrophy. Objective: Investigate the effects of telmisartan on angiotensin II-induced cardiomyocyte hypertrophy and the phosphorylation of extracellular signal-regulated kinase (p-ERK1/2) in rat-cultured cardiomyocytes. Methods: Rat myocardial cells were cultured. Beating rates of the cardiomyocytes, cell volumes, total protein contents, protein synthesis rates, and ERK activity were measured. The phosphorylation of p-ERK1/2 was analyzed by Western blot. Results: Treatment of cultured cardiomyocytes with telmisartan inhibited angiotensin II-induced increases in cell volume, beating rate, total protein content and protein synthesis rate. Telmisartan markedly inhibited p-ERK1/2 phosphorylation in a dose- and time-dependent manner. Conclusion: Telmisartan could suppress cardiomyocyte hypertrophy induced by angiotensin II. The mechanism might be related to the inhibition of p-ERK1/2 phosphorylation. Keywords: Angiotensin II, cardiomyocyte hypertrophy, extracellular signal-regulated kinase, telmisartan