Source:http://linkedlifedata.com/resource/pubmed/id/12787339
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2003-6-5
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pubmed:abstractText |
The inhibitory neurotransmission of the stomach was investigated in isolated guinea-pig gastric fundus. In preparations treated with guanethidine (1 micro mol L-1) and p-fluoro-hexahydro-sila-difenidol (1 micro mol L-1), electrical stimulation evoked neurogenic inhibitory responses not modified by hexamethonium (100 micro mol L-1), suggesting that inhibitory postganglionic non-adrenergic non-cholinergic (NANC) nerve fibres are involved. The nitric oxide (NO)-synthase inhibitor Nomega-nitro-l-argininine-methyl-ester hydrochloride (1-100 micro mol L-1) and the soluble guanylyl cyclase inhibitor ODQ (0.1-3 micro mol L-1) also abolished such relaxant response, suggesting the involvement of NO/Cyclic Guanosine 3',5' monophosphate (cGMP) system as the final mechanism of muscle relaxation. The alpha2-adrenoceptor agonist, UK 14 304 (10 nmol L-1-10 micro mol L-1) did not influence the electrical field stimulation (EFS)-evoked NANC responses. These latter responses were also refractory to a variety of receptor agonists and antagonists, acting at Gamma Aminobutyric Acid (GABA), serotonin 5HT1a, opioid micro , delta and kappa, muscarinic M1 and M2, histamine H2 and H3 and cannabinoid receptors. The NANC response was insensitive to the P/Q-type Ca2+-channel blocker omega-agatoxin TK (1 nmol L-1-0.1 micro mol L-1), but partially inhibited by the N-type Ca2+-channel blocker omega-conotoxin GVIA (0.1 nmol L-1-0.1 micro mol L-1), and by the L-type Ca2+-channel blockers nifedipine and calcicludine (0.1 nmol L-1-0.1 micro mol L-1). These data suggest that the NANC relaxation of the isolated guinea-pig gastric fundus is mediated by NO as the final inhibitory (neuro)transmitter at the longitudinal smooth muscle cells. The mechanism(s) promoting NO production is/are Ca2+-dependent, but apparently insensitive to presynaptic modulation. Both N- and L-type channels seem to occur in nitrergic nerve endings, where they contribute to trigger NO diffusion at the synaptic cleft.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Epinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1350-1925
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
15
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
299-306
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12787339-Animals,
pubmed-meshheading:12787339-Calcium Channel Blockers,
pubmed-meshheading:12787339-Calcium Channels,
pubmed-meshheading:12787339-Electric Stimulation,
pubmed-meshheading:12787339-Enteric Nervous System,
pubmed-meshheading:12787339-Enzyme Inhibitors,
pubmed-meshheading:12787339-Epinephrine,
pubmed-meshheading:12787339-Gastric Fundus,
pubmed-meshheading:12787339-Guinea Pigs,
pubmed-meshheading:12787339-Male,
pubmed-meshheading:12787339-Muscle, Smooth,
pubmed-meshheading:12787339-Nerve Fibers,
pubmed-meshheading:12787339-Neural Inhibition,
pubmed-meshheading:12787339-Nitric Oxide,
pubmed-meshheading:12787339-Norepinephrine,
pubmed-meshheading:12787339-Organ Culture Techniques,
pubmed-meshheading:12787339-Presynaptic Terminals
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pubmed:year |
2003
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pubmed:articleTitle |
Prejunctional modulation of non-adrenergic non-cholinergic (NANC) inhibitory responses in the isolated guinea-pig gastric fundus.
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pubmed:affiliation |
Department of Physiology, Bulgarian Academy of Sciences, Sofia, Bulgaria.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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