K(+)-induced dilation of a small renal artery: no role for inward rectifier K+ channels

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.

Lumen diameter and isometric tension recordings have been made from rabbit renal arcuate artery using pressurised- and wire-myography respectively. In addition, conventional whole-cell and amphotericin-perforated patch whole-cell recordings have been made from single smooth muscle cells isolated from the vessel.

Arcuate arteries dilated when the extracellular K+ concentration was raised to 8-10 mM from either zero or a normal physiological level of about 6 mM. The effect was not endothelium-dependent. Application 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 the 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 (-1.44 pA pF-1 at -60 mV). K(+)-induced vasodilation of the arcuate artery was abolished by 10 microM ouabain and the half-effective concentration of K+ which induced vasodilation was 0.9-1.5 mM.

The observations suggest that an increase in the extracellular K+ concentration (up to about 10 mM) dilates the rabbit renal arcuate artery and that the primary mechanism underlying 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.