Centrally Applied Nitric Oxide Donors Inhibit Vagally Evoked Rat Gastric Acid Secretion: Involvement of Sympathetic Outflow
Kunihiko Yokotani, Yoshinori Murakami, Yasunobu Okuma and Yoshitsugu
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