© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Phenylephrine-induced stimulation of Na+/Ca2+ exchange in rat ventricular myocytes
Centre for Experimental Surgery and Anaesthesiology, Katholieke Universiteit Leuven, Provisorium 1, Minderbroederstraat 17, B-3000 Leuven, Belgium
* Corresponding author. Tel.: +32 (16) 337298; Fax: +32 (16) 337855.
Objective: The effect of an 
-adrenergic agonist, phenylephrine, on the Na+/Ca2+ exchange current in rat ventricular myocytes was investigated. Methods: The Na+/Ca2+ exchange current was measured at room temperature in rat ventricular myocytes as the whole-cell current induced by addition of extracellular Na+ and Ca2+, while blocking Na+ current by setting the holding potential at –30 mV, K+ currents by intracellular Cs+, TEA+ and by extracellular Ba2+, Ca2+ current by nifedipine and Na+ pump current by ouabain or by 0 extracellular K+. Results: Under these experimental conditions, application of external Na+ and Ca2+ induced a current which was further increased by phenylephrine. Phenylephrine (80 µM) increased the current by up to 31.0±5.4% of control at all membrane potentials tested both below and above the reversal potential. The reversal potential (+21.0±3.2 mV), which corresponded with the theoretical reversal potential for the Na+/Ca2+ exchange current under our ionic conditions (+21.3 mV), was not changed by phenylephrine (+23.2±4.1 mV). Applying phenylephrine in the absence of Na+/Ca2+ exchange (0 Nae+, 0 Cae2+) did not change the current. The effect was resistant to propranolol, a β-adrenergic blocker, but prevented by prazosin, an -receptor antagonist, by neomycin, an inhibitor of phospholipase C, and by chelerythrine, a selective inhibitor of protein kinase C. Phorbol 12-myristate 13-acetate failed to stimulate the current. The effect remained similar under conditions of high (HEPESi=5 mM) and low (HEPESi=0.5 mM) intracellular pH buffering. Conclusion: Our data indicate that phenylephrine stimulates the Na+/Ca2+ exchange, both in the forward and the reverse modes, probably via a protein kinase C-dependent pathway.
KEYWORDS Experimental; Heart; Electrophysiology; Pharmacology; Adrenergic agonist; Membrane current; Myocyte; Na/Ca exchanger; Protein kinase; Rat
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