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Effects of endogenous and exogenous nitric oxide on gastric alkaline secretion in anesthetized rats


, : Effects of endogenous and exogenous nitric oxide on gastric alkaline secretion in anesthetized rats. Asia Pacific Journal of Pharmacology 9(4): 259-265

The influence of nitric oxide (NO) on gastric HCO-3- secretion was examined using N-G-nitro-L-arginine methyl ester (L-NAME: NO synthase inhibitor) and nitroprusside (NO doner) in the anesthetized rats. The rat stomach was mounted on a chamber, perfused with saline, and HCO-3- secretion was measured at pH 7.0 using a pH-stat method and by adding 10 mM HCl (acid secretion had been inhibited by pretreatment with omeprazole). The HCO-3- secretion was decreased by nitroprusside (4 mg kg-1, i.v.) and increased by L-NAME (1-5 mg kg-1, i.v.), respectively. The stimulatory effect of L-NAME was antagonized by co-administration of L-arginine (200 mg kg-1, i.v.) and nitroprusside (4 mg kg-1, i.v.), whereas the effect of nitroprusside was antagonized by the guanylate cyclase inhibitor methylene blue (10 mg kg-1, i.v.). Nitroprusside (2-8 mg kg-1, i.v.) also caused a significant decrease in the HCO-3- secretory responses induced by not only L-NAME (10 mu-g kg-1 h-1) but also by 16,16-dimethyl prostaglandin E-2 (10 mu-g kg-1 h-1), and this effect was also significantly antagonized by prior administration of methylene blue. These findings suggest that NO has an inhibitory effect on gastric HCO-3- secretion, and this effect may be mediated by the guanylate cyclase-cyclic GMP system. The stimulation by L-NAME of HCO-3- secretion may be in part due to a removal of the inhibitory influence of endogenous NO on this secretion.

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