Alpha-1 adrenoceptors mediate splanchnic nerve inhibition of pentagastrin-induced gastric acid secretion and mucosal blood flow in rats.
Effects of stimulation of the sympathetic nervous system on pentagastrin-induced increases in gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized, gastric fistula rats. Gastric acid secretion and MBF were increased by i.v. infusion of a submaximal dose of pentagastrin (1.0 microgram/kg/min). Stimulation of the splanchnic nerve was carried out under the steady, increased state of pentagastrin-stimulated acid secretion and MBF. Stimulation of the splanchnic nerve significantly reduced gastric acid secretion, while MBF was little affected. Thus, the delta MBF/delta H+ ratio was significantly increased during this stimulation. Phentolamine, but not propranolol, abolished the inhibitory effects of splanchnic nerve stimulation on the pentagastrin-stimulated gastric acid secretion. In addition, prazosin, but not yohimbine, abolished the inhibitory effects of splanchnic nerve stimulation on the pentagastrin-induced gastric acid secretion. These results suggest that splanchnic nerves directly inhibit pentagastrin-induced gastric acid secretion through alpha-1 adrenoceptors, independently of changes in the MBF, in rats.[1]References
- Alpha-1 adrenoceptors mediate splanchnic nerve inhibition of pentagastrin-induced gastric acid secretion and mucosal blood flow in rats. Yokotani, K., Osumi, Y. J. Pharmacol. Exp. Ther. (1986) [Pubmed]
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