Inhibition of endogenous nitric oxide reduces basal mesenteric vascular tone but does not alter intraduodenal hydrochloric acid-induced intestinal hyperemia in rats.

There are conflicting reports on the role of endogenous nitric oxide (NO) in the regulation of basal intestinal blood flow. The effect of inhibition of NO in intraduodenal hydrochloric acid (HCl) induced intestinal hyperemia remains to be confirmed. We investigated the effect of inhibition of endogenous NO on basal intestinal blood flow, HCl-induced intestinal hyperemia, and duodenal villous injury. Superior mesenteric artery blood flow in rats was measured by pulsed Doppler flowmetry and duodenal villous injury evaluated by histology. Intravenous NG-nitro-L-arginine methyl ester (L-NAME), or L-arginine or D-arginine followed by L-NAME, was given to show inhibition, reversal of inhibition of endogenous NO synthase, and stereospecificity, respectively. An intraduodenal 2 ml/kg bolus or perfusion for 30 min of 0.1 N HCl was given 15 min after L-NAME or vehicle. Mean arterial blood pressure was increased by L-NAME, which also significantly reduced intestinal blood flow under basal condition and after intraduodenal HCl. Basal mesenteric blood flow was not altered by L- or D- arginine. The L-NAME-induced increase in blood pressure and decrease in basal blood flow was attenuated by L- but not D-arginine. The villous damage and the magnitude of the peak hyperemia was unchanged by L-NAME, L- or D-arginine. Inhibition of endogenous NO by L-NAME is suggested by the significant rise in blood pressure. The rise in blood pressure and reduction in blood flow are attenuated by L- but not D-arginine, indicating stereospecificity. Inhibition of endogenous NO reduces basal mesenteric vascular tone but does not alter intraduodenal HCl-induced intestinal hyperemia.(ABSTRACT TRUNCATED AT 250 WORDS)