Zk. Krowicki et al., Excitation of dorsal motor vagal neurons evokes non-nicotinic receptor-mediated gastric relaxation, J AUTON NER, 77(2-3), 1999, pp. 83-89
Vagal stimulation results in both gastric motor excitatory and non-adrenerg
ic non-cholinergic (NANC) inhibitory responses. The NANC pathway involves p
reganglionic cholinergic neurons, which act through nicotinic receptors to
ultimately evoke gastric smooth muscle relaxation via release of nitric oxi
de (NO) and other neurotransmitters. Within the dorsal motor nucleus of the
vagus (DMN), some preganglionic neurons also contain NO synthase. The NO s
ynthase-containing neurons innervate the gastric fundus where adaptive rela
xation occurs. This study tests the hypothesis that chemical stimulation of
vagal motor neurons in animals, in which nicotinic receptors are blocked,
evokes an NO-dependent gastric relaxation. A cell body excitant, N-methyl-D
-aspartate (NMDA, 0.03-3 nmol), was microinjected into the DMN in anestheti
zed rats while recording intragastric pressure (IgP). The first group recei
ved NMDA before and after administration of a ganglionic blocker, hexametho
nium bromide (15 mg/kg, i.v.) and atropine (1.0 mg/kg). Significant dose-de
pendent increases in IgP and gastric motility occurred before hexamethonium
after the 0.3 and 3 nmol doses of NMDA. After hexamethonium, 0.3 and 3 nmo
l NMDA evoked significant decreases in IgP. A second group of rats was hexa
methonium-pretreated and received NMDA microinjection into the DMN before a
nd after an NO synthase inhibitor, N-G-nitro-L-arginine methyl ester (10 mg
/kg, i.v.). The NMDA-evoked decrease in IgP was completely abolished by the
NO synthase inhibitor. These data support the novel idea that NO synthase-
containing preganglionic neurons mediate gastric relaxation that is indepen
dent of nicotinic receptors. (C) 1999 Elsevier Science B.V. All rights rese
rved.