Gastric Hyperemia Accompanying Acid Secretion is Not Mediated by Sensory Nerves

Overview

Journal Dig Dis Sci

Specialty Gastroenterology

Date 1993 Jul 1

PMID 8325181

Authors

E H Livingston

P Holzer

Affiliations

Soon will be listed here.

Abstract

It is not known how the signal to increase gastric mucosal blood flow is passed from the gastric parietal cell layer to the resistance vessels in the submucosa. We tested the hypothesis that mucosal hyperemia accompanying stimulated gastric acid secretion is mediated by capsaicin-sensitive sensory nerves. Rats were denervated by systemic capsaicin treatment (125 mg/kg, subcutaneously, 10-14 days prior to experimentation). Acid secretion was stimulated by intravenous pentagastrin (4, 12, and 36 micrograms/kg/hr) and was measured by a continuous perfusion method. Mucosal blood flow was measured by the hydrogen gas clearance method. Sensory denervation did not affect basal blood pressure, gastric acid secretion, or mucosal blood flow. In control rats, increases in gastric mucosal blood flow and acid secretion were dose-related. With denervation, not only was there no inhibition of the blood flow response to acid secretion, but the dose-dependent rise in acid secretion was accompanied by increased mucosal blood flow that was out of proportion to the acid secretory response. The capsaicin-sensitive afferent fibers do not transmit the signal to increase gastric mucosal blood flow in response to stimulated acid secretion. It appears that sensory nerves modulate but do not mediate the mucosal hyperemic response to acid secretion.

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