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.
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