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Contribution of acetylcholine, vasoactive intestinal polypeptide and nitric oxide to CNS‐evoked vagal gastric relaxation in the rat
Author(s) -
KROWICKI Z. K.,
HORNBY P. J.
Publication year - 1996
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/j.1365-2982.1996.tb00269.x
Subject(s) - vasoactive intestinal peptide , acetylcholine , endocrinology , atropine , medicine , cholinergic , chemistry , nitric oxide , nitric oxide synthase , neuropeptide , receptor
Several in vitro models of gastric relaxation have elucidated a role of nitric oxide (NO) and vasoactive intestinal polypeptide (VIP) in non‐adrenergic, non‐cholinergic (NANC) vagally mediated gastric relaxation. However, these models do not necessarily mimic the events leading to gastric relaxation in the whole animal. We have recently described a vagally mediated gastric relaxation evoked by micro‐injection of substance P (SP) into the nucleus raphe obscurus (NRO). The present study was performed to elucidate whether this CNS‐stimulated in vivo gastric relaxation involved acetylcholine, NO and VIP. Atropine (1 mg kg −1 i.v.), reduces both the rapid nadir and sustained gastric relaxation evoked by SP in the NRO, and the residual responses are abolished by N G ‐Nitro‐L‐arginine methyl ester hydrochloride (L‐NAME, 10 mg kg −1 i.v.), an NO synthase inhibitor. Blockade of NO synthase alone is not sufficient to abolish the effect of SP into the NRO on intragastric pressure. A VIP antagonist, [p‐chloro‐D‐Phe 6 , Leu 17 ]VIP (32 μg i.v.) alone, or with the addition of L‐NAME, does not affect the nadir of the gastric relaxation in response to SP microinjected into the NRO; however, both antagonists reduce the CNS‐evoked sustained intragastric pressure relaxation. We conclude that, in CNS‐evoked gastric relaxation, inhibition of cholinergic pathways is potentially important for both the rapid nadir and sustained gastric relaxation, and both NO and VIP contribute to sustained gastric relaxation.