ABSTRACT
The possibility that extracellular K + ions represent E D H F was explored in main and small mesenteric and in small gastric arteries of the rat. The membrane potential of the smooth muscle cells was measured with conventional microelectrodes in the continuous presence of N G -nitro-L-arginine and indomethacin. In the main mesenteric artery, inhibition of the inward rectifier with low concentrations of barium, which slightly depolarized the smooth muscle cells, did not affect the peak endothelium-dependent hyperpolarization induced by superfusion with acetylcholine. In small mesenteric arteries, in which barium depolarized the smooth muscle cells to a larger extent, the endothelium-dependent hyperpolarization to acetylcholine was increased. The addi tional application of a high concentration of ouabain further depolarized the smooth muscle cells of both arteries. In the combined presence of barium plus ouabain, the hyperpolarization elicited by acetylcholine was not abolished but decreased to 64% of the control response in the main arteries, and not significantly affected in small mesenteric arteries. Measurements with K + ion-selective microelectrodes did not reveal a rise in subendothelial K + activity in main mesenteric arteries during stimulation with acetylcholine. Increasing the K + concentration in the superfusate depolarized the smooth muscle cells of main and small mesenteric and of small gastric arteries. These findings argue against a role of smooth muscle inward rectifier K + channels and N a / K pumping in the acetylcholine-induced endothelium-dependent hyperpolarization in the studied blood vessels.
