Role of nitric oxide in gastric hyperemia induced by central vagal stimulation

Abstract

The effects of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, on the vagal cholinergic increase in gastric mucosal blood flow (GMBF) and acid secretion induced by intracisternal injection of the thyrotropin-releasing hormone (TRH) analogue, RX 77368, were studied. GMBF and acid secretion were measured simultaneously by the hydrogen gas clearance technique and titration of gastric perfusate in urethan-anesthetized rats. RX 77368 (30 ng) injected intracisternally stimulated gastric acid secretion and GMBF for 90 and 180 min respectively. GMBF was increased from basal 63 +/- 4 to 166 +/- 14 ml.min-1.100 g-1 at 60 min postinjection. L-NAME (3 mg/kg) injected intravenously 15 min before RX 77368 completely prevented the increase in GMBF induced by the TRH analogue, whereas the acid response was not modified. The effect of L-NAME was reversed by L-arginine but not by the stereoisomer D-arginine. These results show that the increase in GMBF, but not the stimulation of acid secretion, induced by central vagal activation is mediated through a product of L-arginine-NO pathway.

Cephalic phase of acid secretion involves activation of medullary TRH receptor subtype 1 in rats

“…TRH delivered to DMN neurons or injected intracisternally stimulates the activity of preganglionic vagal motor neurons, gastric vagal efferent fibers, and gastric myenteric neurons (32,34,51). This results in a vagal cholinergicdependent stimulation of gastric acid secretion, motility, emptying, and mucosal blood flow in rats and cats (15,46,49). TRH actions in the brain are mediated by an interaction with two TRH receptors, subtypes 1 (TRH 1 ) and 2 (TRH 2 ) (5, 6).…”

The Role of Capsaicin-Sensitive Afferent Nerves in Gastric Mucosal Protection Initiated Centrally or Peripherally under Experimental Conditions

“…The process is likely to be vagal dependent, and biochemical and pharmacological studies have shown that vagal cholinergic pathway stimulates gastric prostaglandin and nitric oxide release. In addition, vagal muscarinic mediated release of prostaglandins, histamine and serotonin [147,150] evoke sensory C-fiber excitation and a subsequent release of neuropeptides from sensory nerve endings.…”

“…), which induces ablation of primary sensory neurons and the depletion of CGRP-containing fibers, pharmacological blockade of peripheral CGRP 1 receptors by hCGRP 8-37 and NO synthesis by NO-synthase inhibitor N ω -nitro-L-arginine methyl ester blocked the increased gastric mucosal blood flow induced by i.c. injection of TRH [149][150][151][152][153]. The results indicate that the intact function of sensory fibers containing CGRP and NO is basically important for stimulation of gastric mucosal blood flow and the consequent gastroprotection [152], and the CGRP/NO-mediated gastric hyperemia plays a crucial role to withstand gastric mucosal damage [reviews 61,154].…”

Role of the Sympathetic Nervous System in Gastric Functional Changes Induced by Thyrotropin-Releasing Hormone in Rats

“…The mechanism by which TRH increases GMBF is postulated to involve the release of nitric oxide or prostaglandins through vagal stimulation (5,20,21). If TRH activates the sympathetic nervous system, it would be rational that the increase in GMBF in response to TRH should be potentiated by pretreatment with a-blockers because of the removal of the suppression by the sympathetic nervous system.…”