γ-Aminobutyric acid and gastric acid secretion: A physiologic role?

Abstract

The purpose of this study was to examine the effect of endogenous brain GABA levels or GABAergic tone on gastric acid secretion. Experiments were performed with Sprague-Dawley rats under urethane anesthesia. Continuous acid secretion was measured in vivo using a gastric luminal perfusion system. Initial experiments studied the effects on basal acid secretion of (aminooxy)acetic acid (AOAA), a substance which increases brain GABA levels, and flumazenil, a substance which decreases central GABAergic neurotransmission. After basal acid secretion was measured for 30 min, AOAA (15 mg/kg), flumazenil (10 mg/kg), or saline was given by intravenous infusion and acid secretion was measured for 120 min. There was no significant difference in acid secretion between groups ( n = 8/group). A second series of experiments measured the effects of AOAA, flumazenil, or saline on gastric secretion during submaximal stimulation by bethanechol (180 μg/kg/hr) in normal and vagotomized rats. Total acid secretions (mean ± SE) after saline, AOAA, or flumazenil were 78.7 ± 11.8, 51.0 ± 5.9, and 109.3 ± 1.5 μmole/90 min, respectively ( P < 0.01). In vagotomized rats, there were no significant differences in rates of acid secretion between groups. In summary, GABAergic tone did not effect basal acid secretion in anesthetized rats. However, during submaximal acid secretion, acid secretion decreased when brain GABA levels increased, and acid secretion increased when GABAergic neurotransmission was inhibited. We conclude that endogenous brain GABA levels may effect gastric acid secretion in rats, perhaps via inhibition of central—vagal tone.