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Am J Physiol Heart Circ Physiol 265: H2184-H2195, 1993;
0363-6135/93 $5.00
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AJP - Heart and Circulatory Physiology, Vol 265, Issue 6 2184-H2195, Copyright © 1993 by American Physiological Society

ARTICLES

Metabolic inhibition enhances Ca(2+)-activated K+ current in smooth muscle cells of rabbit portal vein

A. L. Miller, E. Morales, N. R. Leblanc and W. C. Cole
Department of Physiology, St. Boniface Research Centre, University of Manitoba, Winnipeg, Canada.

The effect of metabolic inhibition on macroscopic and single-channel K+ currents in isolated rabbit portal vein myocytes was investigated by patch-clamp technique. Depression of adenosine triphosphate synthesis was produced by 2-deoxy-D-glucose (10 mM) and either cyanide (2 mM) or dinitrophenol (50 microM). Outward quasi-steady-state current evoked by a ramp protocol and outward time-dependent current during step depolarizations were increased during metabolic inhibition. The reversal potential for quasi-steady-state current shifted negatively toward equilibrium potential of K+ during treatment consistent with a role for K+ conductance and hyperpolarization of membrane potential. The macroscopic K+ current affected was 1) voltage dependent, 2) inhibited by intracellular Ca2+ chelation and low tetraethylammonium ion (1 mM) but unaffected by 4-aminopyridine (2 mM), and 3) associated with a rise in intracellular Ca2+ assessed by indo 1. Metabolic inhibition caused an increase in voltage-dependent large-conductance K+ channel (120-130 pS) activity in cell-attached patches of myocytes bathed in physiological solution (140 mM K+ in pipette). The channels were blocked in a flickery fashion by tetraethylammonium ion (0.5 mM) and inhibited with charybdotoxin (100 nM). We conclude that metabolic inhibition increases the activity of large-conductance Ca(2+)-activated K+ channels in vascular smooth muscle.


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