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Vasodilator responses to nitric oxide are enhanced in mesenteric arteries of portal hypertensive rats
Author(s) -
HEINEMANN A.,
STAUBER R. E.
Publication year - 1996
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1996.2340557.x
Subject(s) - dilator , portal hypertension , vasodilation , nitric oxide , medicine , splanchnic , acetylcholine , forskolin , mesenteric arteries , hyperdynamic circulation , endocrinology , sodium nitroprusside , hyperaemia , cardiology , anesthesia , artery , hemodynamics , blood flow , cirrhosis , stimulation
Abstract. Nitric oxide (NO) is discussed as a mediator of the splanchnic hyperaemia in portal hypertension. We assessed the vasorelaxation by the NO‐dependent vasodilator acetylcholine, the NO donor 3‐morpholino‐sydnonimine (SIN‐1) and forskolin, a stimulator of the adenylate cyclase pathway in potassium‐preconstricted isolated perfused mesenteric arteries of portal vein‐ligated and sham‐operated rats. Dilator responses to acetylcholine and SIN‐1 were significantly enhanced in vessels of portal vein‐ligated rats as compared to sham‐operated rats, whereas no difference was found in forskolin‐induced vasodilatation. This suggests enhanced reactivity of the vasculature to NO in experimental portal hypertension.