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Am J Physiol Cell Physiol 256: C1131-C1137, 1989;
0363-6143/89 $5.00
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AJP - Cell Physiology, Vol 256, Issue 6 C1131-C1137, Copyright © 1989 by American Physiological Society

ARTICLES

Isoproterenol, DBcAMP, and forskolin inhibit cardiac sodium current

K. Ono, T. Kiyosue and M. Arita
Department of Physiology, Medical College of Oita, Japan.

We studied the effects of isoproterenol (ISP), dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), and forskolin on the sodium current (INa) of guinea pig ventricular myocytes using the tight-seal, whole cell voltage-clamp method. The extracellular [Na+] [( Na+]o) was decreased to 60 mM by replacing NaCl with sucrose (temperature, 32-33 degrees C). Ionic currents other than Na+ were suppressed using appropriate channel blockers. Depolarizing clamp pulse (duration, 30 ms) was applied at a rate of 0.2 Hz from a holding potential of -80 mV. ISP (1 microM) decreased the peak INa by 34% from 6.1 +/- 1.9 (SD) nA (control) to 4.0 +/- 1.5 nA (n = 7). The inhibition was more prominent at less negative potentials and disappeared in the presence of a beta-blocker (10 microM atenolol). The effects of DBcAMP (1-5 mM) and forskolin (3 microM) mimicked those of ISP and depressed the peak INa reversibly. DBcAMP (5 mM) shifted the inactivation curve of INa [h infinity-membrane potential (Em) relationship] to a hyperpolarizing direction, by 3.4 +/- 0.8 mV (n = 5). These findings suggest that ISP inhibits the cardiac INa+, probably by altering the gating mechanism of the Na+ channel, and that the effect is secondary to the increased levels of intracellular cAMP, with possible acceleration of cAMP-dependent phosphorylation of the channel.


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