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Am J Physiol Heart Circ Physiol 275: H577-H590, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 2, H577-H590, August 1998

Electrophysiological properties of neonatal rat ventricular myocytes with alpha 1-adrenergic-induced hypertrophy

John P. Gaughan, Colleen A. Hefner, and Steven R. Houser

Department of Physiology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140

The electrophysiology of neonatal rat ventricular myocytes with and without hypertrophy has not been characterized. The alpha 1-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 alpha -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 alpha 1-adrenergic pathway and caused electrophysiological changes and effects on ion channel expression.

electrophysiological changes; ion channels


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