K-INDUCED DILATION OF A SMALL RENAL-ARTERY - NO ROLE FOR INWARD RECTIFIER K+ CHANNELS()

Objective: To investigate the mechanism of K+-induced vasodilation in a small artery from the kidney, with a particular emphasis on the role of inward rectifier K+ channels. Methods: Lumen diameter and isometri c tension recordings have been made from rabbit renal arcuate artery u sing pressurised-and wire-myography respectively. In addition, convent ional whole-cell and amphotericin-perforated patch whole-cell recordin gs have been made from single smooth muscle cells isolated from the ve ssel. Results: Arcuate arteries dilated when the extracellular K+ conc entration was raised to 8-10 mM from either zero or a normal physiolog ical level of about 6 mM. The effect was not endothelium-dependent. Ap plication of 0.01-1 mM Ba2+ to block inward rectifier K+ channels had no significant effect on K+-induced vasodilation in the arcuate artery , but under the same experimental conditions K+-induced dilation of th e rat posterior cerebral artery was abolished by Ba2+. In the presence of 60 mM extracellular K+, inward rectifier K+-current was detectable in some single smooth muscle cells isolated from arcuate arteries but on average the current density was low (-1.41 pA pF(-1) at -60 mV). K +-induced vasodilation of the arcuate artery was abolished by 10 mu M ouabain and the half-effective concentration of K+ which induced vasod ilation was 0.9-1.5 mM. Conclusions: The observations suggest that an increase in the extracellular K+ concentration (up to about 10 mM) dil ates the rabbit renal arcuate artery and that the primary mechanism un derlying the effect may be stimulation of Na+-K+ ATPase in the smooth muscle cell membrane. Inward rectifier K+ channels have a low average density in smooth muscle cells isolated from arcuate arteries and play no significant role in K+-induced vasodilation. (C) 1998 Elsevier Sci ence B.V.