[Neuropharmacological studies on the sympathetic inhibitory mechanisms of gastric acid secretion].
The inhibitory mechanism of the gastric acid secretion by the sympatho-adrenomedullary system was examined by electrical stimulation of the greater splanchnic nerves of urethane-anesthetized rats with gastric fistula. Stimulation of the greater splanchnic nerve or adrenal branch of the splanchnic nerve reduced both vagally stimulated acid secretion and mucosal blood flow (MBF). On the other hand, after cutting the adrenal branch, selective stimulation of the postganglionic splanchnic nerve (SP) reduced the vagally stimulated acid secretion without affecting MBF. These direct inhibitions by SP nerve stimulation were also observed in the bethanechol- and pentagastrin-induced acid secretion, but not in the histamine-induced acid secretion. SP-induced inhibition on the vagally stimulated acid secretion was abolished by phentolamine and yohimbine. On the other hand, SP-induced inhibitions on the bethanechol- and pentagastrin-induced acid secretion were abolished by phentolamine and prazosin. From these observations, gastric sympathetic nerves directly inhibit the gastric acid secretion by activation of adrenergic alpha-1 and -2 adrenoceptors, alpha-2 adrenoceptors on the parasympathetic neurons in the gastric wall, and alpha-1 adrenoceptors on the structures near the parietal cells.
Yokotani
K
K
Department of Pharmacology, Kochi Medical School, Japan.
D000818:Animals; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000098:blood supply; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D012039:Regional Blood Flow; D013153:Splanchnic Nerves / Q000502:physiology; D013270:Stomach / Q000294:innervation*; D013564:Sympathetic Nervous System / Q000502:physiology*
D011942:Receptors, Adrenergic, alpha