| Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1986: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1985: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Research Abstract |
1. In the urethane-anesthetized rats, electrical stimulation of the splanchnic nerve, gastric sympathetic nerve, reduced histamine-stimulated gastric acid secretion and mucosal blood flow (MBF). This inhibition of acid secretion and MBF was abolished by phentolamine, an alpha-adrenoceptor blocking agent, but not by propranolol, a beta-adrenoceptor blocking agent.
2. In urethane-anesthetized rats, increased release of histamine and 1-methyl histamine, a metabolite of histamine, into gastric juice and portal vein was not observed during infusion of bethanechol, a cholinergic muscarinic receptor agonist, or pentagastrin. Furthermore, in in vitro experiment with perfusion of gastric mucosa, these agents also could not increase the release of histamine and its metabolite.
Previously, we showed that electrical stimulation of the splanchnic nerve reduced the bethanechol- and pentagastrin-induced gastric acid secretion without reduction of MBF, through alpha-1 adrenoceptor-mediated mechanisms. On the other hand, inhibition of histamine-induced acid secretion by stimulation of the splanchnic nerve, in the present study, was secondary to a reduction of MBF. Thus, a possibility that alpha-1 adrenoceptors located on the histamine-containing cells reduce the release of histamine was raised. But, in the present experiment, the release of histamine was not enhanced by bethanechol or pentagastrin. From these results, it is suggested that alpha-1 adrenoceptors locate on parietal cells, thereby reducing bethanechol- and pentagastrin-induced acid secretion in rats.
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