Vagal Release of Gastrin in Cats Following Reserpine¹

Abstract

Abstract Reserpine treatment of nonanesthetized cats has previously been shown to sensitize the HCl‐secreting cells to injected gastrin, probably by a centrally induced enhancement of vagal tone. Indications were obtained also of an interference with the gastrin mechanism. Since vagal impulses are considered to be able to release gastrin, the effect of reserpine on the gastrin activity of the antral and duodenal mucosa has been investigated. Gastrin was extracted from the mucosae of reserpine‐injected and untreated cats and the secretory activity of the preparations determined on nonanesthetized gastric nstula cats. An intramuscular injection of 0.10 mg of reserpine per kg b. w. reduced the gastrin activity of the antral mucosa by about 60 per cent in 24 hrs. Neither a 20‐fold increase in dose nor repetition of the injection of 0.10 mg per kg every 24 hrs for 2 or 4 days produced any further reduction and the gastrin activity returned to normal level despite repeated injections for 8 days. An intravenous infusion of 0.03 mg of reserpine per kg, which produces gastric hypersecretion of acid for several hours, caused no significant alteration in the gastrin activity of the antral mucosa. The gastrin activity of the duodenal mucosa amounted to about one‐tenth the activity of the antral mucosa and was reduced by 0.10 mg of reserpine i. m. daily for 2 or 4 days. Bilateral vagotomy did not alter the gastrin activity of either the antral or doudenal mucosa nor did the i. m. injection of 0.10 mg of reserpine per kg daily for 2 days in vagotomized cats. It is suggested that reserpine causes release of antral and duodenal gastrin by central vagal activation. The significance of gastrin release as a mechanism by which reserpine activates the HCl‐secreting cells is discussed.