Role of the sympathetic nervous system in gastric functional changes induced by thyrotropin-releasing hormone in rats

We determined the changes in gastric functions and systemic blood pressure in response to thyrotropin-releasing hormone (TRH) simultaneously in anesthetized rats and examined the role of the sympathetic nervous system in these changes. TRH injected i.c. increased gastric acid secretion, contraction and mucosal blood flow, and produced hemorrhagic lesions in the glandular stomach. These responses to TRH were almost completely inhibited by bilateral cervical vagotomy or atropine. The increased gastric acid secretion and contraction in response to TRH were significantly augmented by pretreatment with yohimbine but not with prazosin. Bilateral adrenalectomy also potentiated the gastric acid secretory and contractile responses to TRH. Neither prazosin, yohimbine nor adrenalectomy had any appreciable effect on the increased gastric mucosal blood flow induced by TRH. TRH-induced gastric mucosal lesions were significantly aggravated by yohimbine and adrenalectomy. In vagotomized rats, TRH significantly suppressed the gastric functional changes induced by electrical stimulation of the vagus nerves. These data suggest that while gastric functional changes and mucosal lesions induced by TRH mainly occur through stimulation of the vagus nerves, these responses are extensively modified by the sympathetic nervous system including the adrenal glands.