Existence of NO-triggered vagal afferent activation in the rat gastric mucosa.

AIM

We previously reported the possible involvement of mucosal nitric oxide (NO)-triggered 5-HT release in luminal glutamate sensing by the gastric vagus nerve, and we proposed that the stomach, like the duodenum, could "taste" luminal nutrients. Nitric oxide synthase (NOS) is widely distributed in the gastric mucosa, but the physiological role of mucosal NO is not well understood. In this study, we investigated the functional coupling of NO and vagal nerve endings in the gastric mucosa.

MAIN METHODS

For electrophysiological recordings, male Sprague-Dawley rats were anesthetized with urethane, and afferent nerve responses of rat vagal gastric branches to a NO donor were monitored.

KEY FINDINGS

Intravenous application of 100microg/kg sodium nitroprusside (SNP) transiently increased afferent nerve discharges of the rat ventral gastric vagus, which was followed by rapid changes in blood pressure. High doses of SNP (>300microg/kg, i.v.) showed a biphasic increase in afferent discharges. Secondary activation of the vagal afferent continued even after blood pressure returned to basal levels. SNP-evoked afferent responses were abolished by mucosal 5-HT depletion using p-cholorophenylalanine and were inhibited by pre- and post-treatment with the 5-HT(3) antagonist granisetron.

SIGNIFICANCE

These pharmacological results strongly indicate that NO-triggered 5-HT release is coupled to vagal afferent activation in the rat gastric mucosa.