Extracellular K+-induced hyperpolarizations and dilatations of rat coronary and cerebral arteries involve inward rectifier K+ channels

1. The hypothesis that inward rectifier K+ channels are involved in the vasodilatation of small coronary and cerebral arteries (100-200 mu m diameter) in response to elevated [K+](o) was tested. The diameters and membrane potentials of pressurized arteries from rat were measured using a video-imaging system and conventional microelectrodes, respectively. 2. Elevation of [K+](o) from 6 to 16 mM caused the membrane potential of pressurized (60 mmHg) arteries to hyperpolarize by 12-14 mV. Extracellular Ba2+ (Ba-o(2+)) blocked K+-induced membrane potential hyperpolarizations at concentrations (IC50, 6 mu M) that block inward rectifier K+ currents in smooth muscle cells isolated from these arteries. 3. Elevation of [K+](o) from 6 to 16 mM caused sustained dilatations of pressurized coronary and cerebral arteries with diameters increasing from 125 to 192 mu m and 110 to 180 mu m in coronary and cerebral arteries, respectively. Ba-o(2+) blocked K+-induced dilatations of pressurized coronary and cerebral arteries (IC50, 3-8 mu m). 4. Elevated [K+](o)-induced vasodilatation was not prevented by blockers of other types of K+ channels (1 mM 4-aminopyridine, 1 mM TEA(+), and 10 mu m glibenclamide), and blockers of Na+-K+-ATPase. Elevated [K+](o)-induced vasodilatation was unaffected by removal of the endothelium. 5. These findings suggest that K-o(+) dilates small rat coronary and cerebral arteries through activation of inward rectifier K+ channels. Furthermore, these results support the hypothesis that inward rectifier K+ channels may be involved in metabolic regulation of coronary and cerebral blood flow in response to changes in [K+](o).