Abstract
Experiments were carried out to investigate the interaction between nitric oxide (NO) and cholinergic neurotransmission in smooth muscle strips of guinea-pig gastric fundus. Electrical field stimulation (2 Hz, 1 ms, 360 shocks) evoked atropine-sensitive contractions. Dimethylphenylpiperazinium (DMPP) (100 μM), a nicotinic receptor agonist, reversed the stimulation-evoked contraction and resulted in relaxation. Nω-nitro-L-arginine (L-NNA) (100 μM), an NO synthase inhibitor, significantly increased the amplitude of stimulation-evoked contraction and abolished the effect of DMPP. Electrical stimulation increased the release of [ 3H]acetylcholine ([ 3H]ACh) from the tissue strips above the basal levels. Neither L-NNA (100 μM) nor DMPP (100 μM) alone influenced the basal release of [ 3H]ACh. Nω-nitro-L-arginine (100 μM) decreased the electrical stimulation-evoked release of [ 3H]ACh. Dimethylphenylpiperazinium increased the stimulation-evoked release of [ 3H]ACh but had no effect in the presence of L-NNA. It is suggested that 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 smooth muscle responses to ACh.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
