Endothelium-dependent vasorelaxation independent of nitric oxide and K release in isolated renal arteries of rats

Abstract

1. We investigated whether K+ can act as an endothelium-derived hyperpolarizing factor (EDHF) in isolated small renal arteries of Wistar-Kyoto rats. 2. Acetylcholine (0.001-3 μM) caused relaxations that were abolished by removal of the endothelium. However, acetylcholine-induced relaxations were not affected by the nitric oxide (NO) synthase inhibitor Nω-nitro-k-arginine methyl ester (k-NAME, 100 μM), by k-NAME plus the soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ, 1 μM) or by k-NAME plus the cyclo-oxygenase inhibitor indomethacin (10 μM). In rings precontracted with high-K+(60 mM) physiological salt solution in the presence of k-NAME, acetylcholine-i..