Abstract
Summary: The endothelium-derived relaxing factor (EDRF), classic nitrovasodilators (nitroglycerin, isosorbide dinitrate, etc.), and molsidomine are generally believed to relax vascular smooth muscle through a similar mechanism, namely a nitric oxide (NO)-mediated stimulation of guanylate cyclase, leading to increased cyclic GMP levels, inducing relaxation. Using precontracted rat aortic rings, we investigated the influence of different agents, known to interact with NO, on the relaxation effects elicited by EDRF (released by acetylcholine), NO (generated from acidified nitrite), nitroglycerin, and SIN-1 (the active metabolite of molsidomine). No significant influence of hydroquinone, hemoglobin, and methylene blue was found on SIN-1-induced relaxations, in spite of a profound inhibitory influence on acetylcholine-and NO-induced relaxations. In contrast to the marked increase in cyclic GMP levels in response to EDRF and nitroglycerin, no increase was found in response to SIN-1. Although it is widely accepted that NO and stimulation of guanylate cyclase are involved in SIN-1-induced relaxations, it must be considered that in rat aorta another mechanism might contribute to the relaxing properties of SIN-1.
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