Key result
Telmisartan inhibited angiotensin II-induced increases in cell volume, beating rate, and protein synthesis in cultured rat cardiomyocytes, likely via inhibition of p-ERK1/2 phosphorylation.
Why the study?
Does telmisartan prevent angiotensin II-induced cardiomyocyte hypertrophy in rat cultured cardiomyocytes?
Does telmisartan prevent angiotensin II-induced cardiomyocyte hypertrophy in rat cultured cardiomyocytes?
Telmisartan suppresses angiotensin II-induced cardiomyocyte hypertrophy in vitro, potentially via inhibition of p-ERK1/2 phosphorylation.
Should not inform clinical decisions on hypertrophy; hypothesis-generating for telmisartan effects on ERK signaling in cardiomyocyte models.
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.
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Wei‐Han Chang (2011) studied Angiotensin II-induced cardiomyocyte hypertrophy. Telmisartan vs. Angiotensin II alone was evaluated on Cardiomyocyte hypertrophy (cell volume, beating rate, total protein content, protein synthesis rate) and p-ERK1/2 phosphorylation. Telmisartan inhibited angiotensin II-induced increases in cell volume, beating rate, and protein synthesis in cultured rat cardiomyocytes, likely via inhibition of p-ERK1/2 phosphorylation.
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