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Am J Physiol Heart Circ Physiol 279: H139-H148, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 1, H139-H148, July 2000

Changes in ionic currents and beta -adrenergic receptor signaling in hypertrophied myocytes overexpressing Galpha q

Sayaka Mitarai, Thomas D. Reed, and Atsuko Yatani

Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267

Transgenic overexpression of Galpha q causes cardiac hypertrophy and depressed contractile responses to beta -adrenergic receptor agonists. The electrophysiological basis of the altered myocardial function was examined in left ventricular myocytes isolated from transgenic (Galpha q) mice. Action potential duration was significantly prolonged in Galpha q compared with nontransgenic (NTG) myocytes. The densities of inward rectifier K+ currents, transient outward K+ currents (Ito), and Na+/Ca2+ exchange currents were reduced in Galpha q myocytes. Consistent with functional measurements, Na+/Ca2+ exchanger gene expression was reduced in Galpha q hearts. Kinetics or sensitivity of Ito to 4-aminopyridine was unchanged, but 4-aminopyridine prolonged the action potential more in Galpha q myocytes. Isoproterenol increased L-type Ca2+ currents (ICa) in both groups, with a similar EC50, but the maximal response in Galpha q myocytes was ~24% of that in NTG myocytes. In NTG myocytes, the maximal increase of ICa with isoproterenol or forskolin was similar. In Galpha q myocytes, forskolin was more effective and enhanced ICa up to ~55% of that in NTG myocytes. These results indicate that the changes in ionic currents and multiple defects in the beta -adrenergic receptor/Ca2+ channel signaling pathway contribute to altered ventricular function in this model of cardiac hypertrophy.

action potential; potassium currents; sodium-calcium exchanger; calcium currents; heart failure; transgenic model


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