Sympathoadrenomedullary system mediation of the prostaglandin E2-induced central inhibition of gastric acid output in rats.

Mechanisms related to the gastric antisecretory action of i.c.v.-administered prostaglandins (PGs) were investigated in urethane-anesthetized rats with gastric fistula. The gastric acid output was enhanced by electrical stimulation of the left cervical vagus nerve after cutting the bilateral cervical vagus nerves. Intracerebroventricular administered PGE2 (0.05-0.5 microgram/animal) dose-dependently inhibited the vagally stimulated acid output whereas the same doses of PGE2 administered i.v. were without effect. The inhibitory effect of PGE2 (0.1 microgram/animal, i.c.v.) was more potent than the effects of the same doses of PGD2 and PGF2 alpha (PGE2 greater than PGD2 greater than PGF2 alpha). PGE2 (0.1 microgram/animal)-induced inhibition of the gastric acid output was abolished by splanchnicectomy, cutting the preganglionic splanchnic nerves under diaphragm, or by combined pretreatment with adrenalectomy and 6-hydroxydopamine (50 mg/kg i.v., 3 days before). This PGE2-induced inhibition was also abolished by pretreatment with phentolamine (5 mg/kg i.m.), but not by propranolol (5 mg/kg i.m.). These observations suggest that the i.c.v.-administered PGs, in particular PGE2, induces a central excitation of the sympathoadrenomedullary outflow and that the resultant activation of gastric alpha adrenoceptors inhibits the vagally stimulated gastric acid output.