alpha- 1 and alpha-2 type adrenoceptors involved in the inhibitory effect of splanchnic nerves on parasympathetically stimulated gastric acid secretion in rats.

The inhibitory effects of the splanchnic nerve on the parasympathetically stimulated gastric acid secretion were analyzed using two different types of alpha adrenergic blocking agents (prazosin and yohimbine). When the gastric acid secretion was increased by infusion of bethanechol, a muscarinic parasympathetic stimulant, the inhibitory effect of stimulation of the splanchnic postganglionic (SP) nerve on the gastric acid secretion was abolished by prazosin, but not by yohimbine. On the other hand, when the gastric acid secretion was increased by stimulation of the vagus nerve, the inhibitory effect of stimulation of the SP nerve on the gastric acid secretion was not abolished by prazosin, but was markedly attenuated by yohimbine. Infusion of clonidine had no effect on the bethanechol-induced gastric acid secretion but did inhibit the vagally stimulated gastric acid secretion in a dose-dependent manner. This effect of clonidine on the vagally stimulated gastric acid secretion was selectively abolished by yohimbine. These results suggest that the SP nerve inhibits the bethanechol-induced gastric acid secretion through alpha-1 type adrenoceptors and inhibits the vagally stimulated gastric acid secretion through alpha-2 type adrenoceptors. We propose that alpha-1 type adrenoceptors are located on the structures peripheral to the parasympathetic nerve terminals, whereas alpha-2 type adrenoceptors are located on the vagally stimulated pathways in the gastric wall. The vagally stimulated pathways display paradoxical resistance to the alpha-1 antagonist, prazosin.