Centrally Applied Nitric Oxide Donors Inhibit Vagally Evoked Rat Gastric Acid Secretion: Involvement of Sympathetic Outflow
Kunihiko Yokotani, Yoshinori Murakami, Yasunobu Okuma and Yoshitsugu
Osumi
Department of Pharmacology, Kochi Medical School, Nankoku, Kochi 783,
Japan
Abstract: Intracerebroventricularly (i.c.v.) administered nitric
oxide (NO) donors, 3-morpholinosydnonimine (SIN-1) (100 - 500 microg/animal)
and sodium nitroprusside (SNP) (100 - 250 microg/animal) dose-dependently
inhibited the rat gastric acid secretion evoked by vagal stimulation at
3 Hz. Furthermore, the inhibitory effect of SIN-1 (250 microg/animal) was
more marked and its onset was more rapid than that of SNP (250 microg/animal).
The SIN-1 (250 microg/animal)-induced antisecretory effect was abolished
by both splanchnicotomy and phentolamine (5 mg/kg, i.m.), and also by indomethacin
(500 microg/animal, i.c.v.). These results suggest that i.c.v. administered
NO donors inhibit vagally evoked gastric acid secretion by activation of
central sympathetic outflow. Central prostaglandin is probably implicated
in this NO-mediated antisecretory effect.
Keywords: Gastric acid secretion, Nitric oxide, Sympathetic nervous system