Electrophysiological properties of neonatal rat ventricular myocytes with a1-adrenergic-induced hypertrophy

Gaughan, John P., Colleen A. Hefner, and Steven R. Houser. Electrophysiological properties of neonatal rat ventricular myocytes with a1-adrenergic-induced hypertrophy. Am. J. Physiol. 275 (Heart Circ. Physiol. 44): H577–H590, 1998.—The electrophysiology of neonatal rat ventricular myocytes with and without hypertrophy has not been characterized. The a1-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 Ca21 current in control after 48 h in culture, but current density was significantly less in hypertrophy (24.7 6 0.8 hypertrophy vs. 210.7 6 1.2 control pA/pF, n 5 22, P , 0.05). T-type Ca21 current density was not different. The a-adrenergic antagonist prazosin blocked the hypertrophy and the chronic effect of phenylephrine on L-type Ca21 current. Transient outward K1 current density was decreased 70% in hypertrophy and was blocked with 4-aminopyridine. No change in Na1 current density was observed. Staurosporine, a protein kinase C inhibitor, eliminated the hypertrophy and the effect on L-type Ca21 current. These studies showed that phenylephrineinduced hypertrophy occurred via the a1-adrenergic pathway and caused electrophysiological changes and effects on ion channel expression.