ENDOGENOUS NITRIC-OXIDE IN THE REGULATION OF GASTRIC-ACID SECRETION, GASTRIN-RELEASE AND BLOOD-FLOW

Nitric oxide (NO) was shown to mediate gastric hyperemia following sec retory stimulation but its role in the control of gastric secretion ha s not been elucidated. This study was designed to determine the role o f NO in the regulation of gastric acid secretion and gastrin release i n conscious dogs with chronic gastric fistula and Heidenhain pouch in which the changes in gastric blood flow were measured by laser Doppler flowmetry. Infusion of N-G-nitro-L-arginine (L-NNA), a potent inhibit or of nitric oxide synthase (NOS), failed to affect basal gastric secr etion or plasma gastrin level but suppressed an increase of this secre tion by ordinary meat feeding or i.v. infusion of pentagastrin (4 mu g /kg-h). In tests with feeding infusion of L-NNA caused a significant r eduction in plasma gastrin levels. The inhibition by L-NNA of secretor y response to pentagastrin or feeding was accompanied by a decline in blood flow. Addition of L-arginine to i.v. infusion significantly atte nuated the L-NNA-induced inhibition of gastric secretion and the reduc tion in plasma gastrin response as well as in the fall of gastric bloo d flow. We conclude that endogenous NO affects the gastric secretion a nd this is mediated, in part, by the changes in gastrin release and ga stric micro circulation.