Centrally Applied Nitric Oxide Donors Inhibit Vagally Evoked Rat Gastric Acid Secretion: Involvement of Sympathetic Outflow

Abstract

Intracerebroventricularly (i.c.v.)administered nitric oxide (NO)donors, 3-morpholinosydnonimine (SIN-1)(100-500 μg/animal)and sodium nitroprusside (SNP)(100-250 μg/animal)dosedependently inhibited the rat gastric acid secretion evoked by vagal stimulation at 3 Hz. Furthermore, the inhibitory effect of SIN-1 (250 μg/animal)was more marked and its onset was more rapid than that of SNP (250 μg/animal). The SIN-1 (250 μg/animal)-induced antisecretory effect was abolished by both splanchnicotomy and phentolamine (5 mg/kg, i.m.), and also by indomethacin (500 μg/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 NOmediated antisecretory effect.