Electrophysiological properties of neonatal rat ventricular myocytes with α1-adrenergic-induced hypertrophy.

The electrophysiology of neonatal rat ventricular myocytes with and without hypertrophy has not been characterized. The α1-adrenergic agonist phenylephrine induced hypertrophy in neonatal rat ventricular myocytes. After 48 h of exposure to 20 μM phenylephrine, cell surface area of hypertrophied myocytes was 44% larger than control. Action potential duration was significantly longer in hypertrophy than in control. There was an increase in L-type Ca2+ current in control after 48 h in culture, but current density was significantly less in hypertrophy (-4.7 ± 0.8 hypertrophy vs. -10.7 ± 1.2 control pA/pF, n = 22, P < 0.05). T-type Ca2+ current density was not different. The α-adrenergic antagonist prazosin blocked the hypertrophy and the chronic effect of phenylephrine on L-type Ca2+ current. Transient outward K+ current density was decreased 70% in hypertrophy and was blocked with 4-aminopyridine. No change in Na+ current density was observed. Staurosporine, a protein kinase C inhibitor, eliminated the hypertrophy and the effect on L-type Ca2+current. These studies showed that phenylephrine-induced hypertrophy occurred via the α1-adrenergic pathway and caused electrophysiological changes and effects on ion channel expression.