Abstract
Studies were designed to determine the extent of the involvement of endothelium-derived relaxing factor(s) other than nitric oxide (NO) in vascular relaxation in response to acetylcholine (ACh) in the rabbit renal artery. ACh (10 −9−10 −6M) induced concentration-dependent relaxation of isolated endothelium-intact arterial rings preconstricted with noradrenaline. N G-nitro- l-arginine methyl ester ( l-NAME), an inhibitor of NO synthase, partly inhibited the ACh-induced endothelium-dependent relaxation, whereas it almost completely abolished the production of cyclic-3′, 5′-guanosine monophosphate (cGMP) in these rings in response to ACh. Methylene blue, an inhibitor of guanylate cyclase, had an essentially similar effect to l-NAME on the relaxation. Indomethacin, an inhibitor of cyclooxygenase, had no effect. High concentrations of potassium chloride (to inhibit endothelium-dependent hyperpolarization), tetraethylammonium (TEA) or 4-aminopyridine (4-AP), a voltage-dependent or Ca 2+-dependent K + channel blocker, partly inhibited the relaxation while, in contrast, glibenclamide, an ATP-sensitive K + channel blocker, had no effect. Ouabain, an inhibitor of Na +, K +-ATPase, also partly inhibited the ACh-induced relaxation, especially the higher concentration effect. Application of l-NAME together with ouabain, TEA, or a high concentration of potassium chloride completely abolished the relaxation. These results that ACh-induced endothelium-dependent relaxation in the rabbit renal artery is mediated by NO, and by an other factor(s), which relaxes the vascular smooth muscle through opening K + channels other than ATP-sensitive ones, and/or through the activation of a Na +, K +-pump.
Published Version
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