Nitric oxide (NO) increases acetylcholine release from and inhibits smoothmuscle contraction of guinea-pig gastric fundus

Citation
E. Sotirov et al., Nitric oxide (NO) increases acetylcholine release from and inhibits smoothmuscle contraction of guinea-pig gastric fundus, BRAIN RES B, 49(4), 1999, pp. 297-302
Citations number
51
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BRAIN RESEARCH BULLETIN
ISSN journal
0361-9230 → ACNP
Volume
49
Issue
4
Year of publication
1999
Pages
297 - 302
Database
ISI
SICI code
0361-9230(19990701)49:4<297:NO(IAR>2.0.ZU;2-S
Abstract
Experiments were carried out to investigate the interaction between nitric oxide (NO) and cholinergic neurotransmission in smooth muscle strips of gui nea-pig gastric fundus. Electrical field stimulation (2 Hz, 1 ms, 360 shock s) evoked atropine-sensitive contractions. Dimethylphenylpiperazinium (DMPP ) (100 mu M), a nicotinic receptor agonist, reversed the stimulation-evoked contraction and resulted in relaxation. No-nitro-L-arginine (L-NNA) (100 m u M), an NO synthase inhibitor, significantly increased the amplitude of st imulation-evoked contraction and abolished the effect of DMPP. Electrical s timulation increased the release of [H-3]acetylcholine ([H-3]ACh) from the tissue strips above the basal levels. Neither L-NNA (100 mu M) nor DMPP (10 0 mu M) alone influenced the basal release of [H-3]ACh. N omega-nitro-L-arg inine (100 mu M) decreased the electrical stimulation-evoked release of [H- 3]ACh. Dimethylphenylpiperazinium increased the stimulation-evoked release of [H-3]ACh but had no effect in the presence of L-NNA. It is suggested tha t in guinea-pig gastric fundus, endogenous NO released in response to field stimulation has an opposite effect at the pre- and postsynaptic sites: it increases the release of ACh from cholinergic nerve terminals but reduces s mooth muscle responses to ACh. (C) 1999 Elsevier Science Inc.