THE EFFECT OF NITRIC OXIDE SYNTHASE INHIBITOR L-NAME ON GASTRIC AND DUODENAL BICARBONATE (HCO3 1 SECRETION IN EXPERIMENTAL RATS
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Abstract The role of nitric oxide (NO) in the regulation of gastroduodenal (HCo)" secretion was investigated in anaesthetized rats using the nitric oxide biosynthesis inhibitor NG nitro-L-arginine methyl ester (L-NAME). (1-1(205) secretion was measured at pH 7.0 in the stomach in the presence of omeprazole and in the proximal part of duodenum. Intravenous administration of L-NAME (1-5 mg / kg) increased (HCo5) secretion in a dose dependent manner in both the stomach and duodenum with a concomitant elevation of arterial blood pressure. The exogenous nitric oxide donor nitroprusside (4 mg / kg) by itself decreased the rate of (HCo5) secretion and significantly antagonized the (HCo& stimulatory action of L-NAME. Furthermore, the increased (HCo5) secretion caused by L-NAME was significantly attenuated by prior administration of atropine (1 mg/ kg S.C.) or indomethacin (5 mg/ kg S.C.). None of the treatment had any effect on the changes in blood pressure induced by L-NAME. These results suggest that L-NAME stimulate (HCo) secretion in the gastroduodenal mucosa. This action is associated with the inhibition of nitric oxide biosynthesis and may be partly dependent on oagalchobinergic innervation and mediated by endogenous pros taglandins.