Adrenergic regulation of distention-induced gastrin release in humans

Abstract

To investigate the possible role of adrenergic nerves in neurally mediated gastrin release, we evaluated the effect of selective adrenergic blockade on the serum gastrin response to gastric distention in healthy human subjects. On separate days, 2 mg of propranolol (β-adrenergic antagonist), 5 mg of phentolamine (α-adrenergic antagonist), or saline (control) was injected intravenously just before distending the stomach with 700 ml of isotonic saline. For 30 min following distention, intragastric pH was kept constant at 5.0 by in vivo titration. Propranolol reduced distention-induced gastrin release by approximately 90% (p < 0.02), whereas phentolamine had no significant effect on the gastrin response to distention. In additional experiments, we evaluated the effect of the same doses of propranolol or phentolamine on the exaggerated gastrin response to gastric distention that occurred during cholinergic blockade with atropine. In the presence of atropine (2.3 μg/kg i.v.), propranolol significantly (p < 0.01) reduced distention-induced gastrin release, whereas phentolamine significantly enhanced the gastrin response to distention (p < 0.01). We conclude that: 1.(1) distention-induced gastrin release was reduced by propranolol, suggesting that gastric distention releases gastrin by a β-adrenergic mechanism and2.(2) distention-induced gastrin release was enhanced by phentolamine, but only in the presence of atropine. Thus, adrenergic nerves appear to regulate the gastrin response to gastric distention in humans: β-adrenergic pathways stimulate gastrin release, and α-adrenergic pathways may inhibit gastrin release under certain circumstances.