Endogenous nitric oxide in the regulation of gastric secretory and motor activity in humans.

Abstract

Studies in animals have shown that nitric oxide (NO) affects gastric secretory and motor functions. However, little information is available about the involvement of this substance in the control of gastric secretory and motor activity in man. This study, performed on 18 healthy, Helicobacter pylori-negative volunteers, was designed to evaluate the role of NO in the control of gastric acid secretion and of gastrin and somatostatin release in response to ordinary feeding (group A) and on gastric motor and electrical activity (group B). Gastric acid secretion was determined by means of intragastric pH-metry before and after feeding with a semi-liquid meal. Plasma levels of gastrin and somatostatin were measured using specific radioimmunoassays. Gastric emptying rate was measured using the 13C-acetate breath test, antral motor activity using a manometric catheter and myoelectric activity using cutaneous electrogastrography. Studies were repeated following pre-treatment with NG-monomethyl-L-Arginine (L-NMMA), L-Arginine (L-Arg) or their combination. L-NMMA delayed the recovery of intragastric pH to the pre-meal value, and suppressed postprandial gastrin release while increasing the plasma somatostatin level. L-Arg did not affect postprandial pH and plasma hormones, but reversed L-NMMA-induced alterations in intragastric pH and in plasma gastrin and somatostatin levels. Both postprandial antral motor activity (motility index) and gastric emptying significantly increased in tests with L-NMMA, but this was not observed when L-NMMA was given in combination with L-Arg or when L-Arg alone was used. The gastric electrical pattern, as measured by cutaneous electrogastrography, was not affected by L-NMMA, L-Arg or their combination. (1) Endogenous NO appears to be involved in the regulation of postprandial gastric acid secretion. This effect may be mediated by the changes in release of gastrin and somatostatin. (2) Endogenous NO delays gastric emptying and antral motor activity without affecting gastric myoelectrical activity.