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Am J Physiol Gastrointest Liver Physiol 276: G1043-G1051, 1999;
0193-1857/99 $5.00
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Vol. 276, Issue 4, G1043-G1051, April 1999

NO overproduction by eNOS precedes hyperdynamic splanchnic circulation in portal hypertensive rats

Reiner Wiest1, Vijay Shah1,2,3, William C. Sessa2, and Roberto J. Groszmann1,3

1 Hepatic Hemodynamic Laboratory, Veterans Affairs Medical Center, West Haven 06516; and 2 Boyer Center for Molecular Medicine and 3 Department of Medicine, Yale University School of Medicine, New Haven, Connecticut 06510

Chronic high blood flow and the hyperdynamic circulatory syndrome in portal hypertension are associated with endothelial constitutive nitric oxide (NO) synthase (eNOS) upregulation and increased NO release. In portal vein-ligated (PVL) rats the splanchnic circulation is not yet hyperdynamic on day 3 postoperatively. In vitro perfused superior mesenteric arteries (SMAs) of day 3 PVL and sham rats were challenged with increasing flow rates or the alpha -adrenoreceptor agonist methoxamine (30 and 100 µM) before and after incubation with the NO inhibitor, Nomega -nitro-L-arginine (L-NNA, 10-4 M). Perfusate NO metabolite (NOx) concentrations were measured by chemiluminescence. PVL rats expressed a significant hyporesponsiveness to increases in flow rate or methoxamine that was overcome by incubation with L-NNA. The PVL vasculature showed significantly higher slopes of NOx production vs. flow-induced shear stress, higher increases in perfusate NOx concentration in response to methoxamine, and higher eNOS protein levels (Western blot) compared with sham rats. In conclusion, eNOS-upregulation and increased NO release by the SMA endothelium occur before the development of the hyperdynamic splanchnic circulation, suggesting a primary role of NO in the pathogenesis of arterial vasodilatation.

vasodilation; endothelial nitric oxide synthase; superior mesenteric artery


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