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Am J Physiol Heart Circ Physiol 259: H14-H22, 1990;
0363-6135/90 $5.00
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AJP - Heart and Circulatory Physiology, Vol 259, Issue 1 14-H22, Copyright © 1990 by American Physiological Society

ARTICLES

Effect of pinacidil on ion permeability in resting and contracted resistance vessels

L. M. Videbaek, C. Aalkjaer, A. D. Hughes and M. J. Mulvany
Department of Pharmacology, University of Aarhus, Denmark.

Pinacidil is thought to cause vasodilatation by opening K+ channels and consequent hyperpolarization. This proposed mechanism of action is based mainly on membrane potential measurements and 42K or 86Rb efflux experiments under resting conditions. We have measured the simultaneous effect of pinacidil on force and membrane potential in resting and norepinephrine-contracted rat mesenteric resistance vessels. Also the effect of pinacidil on 42K and 36Cl efflux and 22Na uptake in the absence and presence of norepinephrine was examined. From the membrane potential and ion flux measurements the ion permeabilities were calculated. In both resting and norepinephrine-contracted vessels, pinacidil caused a large hyperpolarization, the latter situation being associated with an almost complete relaxation. In both resting and norepinephrine-stimulated vessels, pinacidil caused a large increase in K+ permeability and a decrease in Cl-permeability, whereas no significant change of Na+ permeability was found. Our results suggest that pinacidil causes vasodilation due to hyperpolarization. The major cause for the hyperpolarization is an increase in K+ permeability.


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