INHIBITION OF GASTRIC-ACID SECRETION BY STRESS - A PROTECTIVE REFLEX MEDIATED BY CEREBRAL NITRIC-OXIDE

Moderate somatic stress inhibits gastric acid secretion. We have inves tigated the role of endogenously released NO in this phenomenon, Eleva tion of body temperature by 3 degrees C or a reduction of 35 mmHg (1 m mHg = 133 Pa) in blood pressure for 10 min produced a rapid and long-l asting reduction of distension-stimulated acid secretion in the rat pe rfused stomach in vivo. A similar inhibitory effect on acid secretion was produced by the intracisternal (i.c.) administration of oxytocin, a peptide known to be released during stress. Intracisternal administr ation of the NO-synthase inhibitor, N-G-nitro-L-arginine methyl ester (L-NAME) reversed the antisecretory effect induced by all these stimul i, an action prevented by intracisternal coadministration of the NO pr ecursor, L-arginine. Furthermore, microinjection of L-NAME into the do rsal motor nucleus of the vagus nerve reversed the acid inhibitory eff ects of mild hyperthermia, i.v. endotoxin, or i.c. oxytocin, an action prevented by prior microinjection of L-arginine. By contrast, microin jection of L-NAME into the nucleus tractus solitarius failed to affect the inhibitory effects of hyperthermia, i.v. endotoxin, or i.v. endot oxin. Immunohistochemical techniques demonstrated that following hyper thermia there was a significant increase in immunoreactivity to neuron al NO synthase in different areas of the brain, including the dorsal m otor nucleus of the vagus, Thus, our results suggest that the inhibiti on of gastric acid secretion, a defense mechanism during stress, is me diated by a nervous reflex involving a neuronal pathway that includes NO synthesis in the brain, specifically in the dorsal motor nucleus of the vagus.