Endothelin stimulates hypertrophy and contractility in neonatal rat cardiac myocytes, mediated by protein kinase C activation and extracellular calcium influx, respectively.
Hypothesis-generating in neonatal rat myocytes; leaves open endothelin's role in human cardiac remodeling pending further studies.
The effect of endothelin (ET) on rat cardiac myocytes cultured in a serum-free, defined medium was determined. ET simulated cardiac myocyte hypertrophy in a dose-dependent manner as determined by the protein synthesis and cell surface area. Since the myocyte hypertrophy was abolished by H-7, a protein kinase C inhibitor, ET-receptor mediated protein kinase C activation may be involved in cardiac myocyte hypertrophy. At the same time, ET also stimulated myocyte contractility in this medium, and this stimulatory effect was inhibited by nicardipine. This result indicates that the influx of extracellular calcium ion is necessary for the stimulation of contractility induced by ET.
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Suzuki et al. (1990) studied this question.
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