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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2002-5-8
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pubmed:abstractText |
The possible participation of glutamate and NO/cGMP in the pressor response to 5-HT3 receptor activation in the nucleus tractus solitarii (NTS) was investigated using selective antagonists in urethane-anaesthetized rats. Intra-NTS administration of NMDA and non-NMDA receptor antagonists, but not metabotropic glutamate receptor antagonists, markedly reduced (70%) the increase in blood pressure caused by local application of the potent 5-HT3 receptor agonist, 1-(m-chlorophenyl)-biguanide. The 5-HT3 receptor-mediated pressor response was also significantly attenuated by the local blockade of nitric oxide synthase and soluble guanylyl cyclase. These data suggest that ionotropic glutamate receptors and the associated NO/cGMP transduction mechanism contribute downstream to the pressor effect elicited by 5-HT3 receptor stimulation in the NTS.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1-(3-chlorophenyl)biguanide,
http://linkedlifedata.com/resource/pubmed/chemical/1H-(1,2,4)oxadiazolo(4,3-a)-quiloxal...,
http://linkedlifedata.com/resource/pubmed/chemical/7-nitroindazole,
http://linkedlifedata.com/resource/pubmed/chemical/Biguanides,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Excitatory Amino Acid Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Guanylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Indazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Oxadiazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Metabotropic Glutamate,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, N-Methyl-D-Aspartate,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Serotonin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Serotonin, 5-HT3,
http://linkedlifedata.com/resource/pubmed/chemical/Serotonin,
http://linkedlifedata.com/resource/pubmed/chemical/Serotonin Receptor Agonists
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0959-4965
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
7
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pubmed:volume |
13
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
837-41
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11997697-Animals,
pubmed-meshheading:11997697-Biguanides,
pubmed-meshheading:11997697-Blood Pressure,
pubmed-meshheading:11997697-Enzyme Inhibitors,
pubmed-meshheading:11997697-Excitatory Amino Acid Antagonists,
pubmed-meshheading:11997697-Glutamic Acid,
pubmed-meshheading:11997697-Guanylate Cyclase,
pubmed-meshheading:11997697-Indazoles,
pubmed-meshheading:11997697-Male,
pubmed-meshheading:11997697-Neurons,
pubmed-meshheading:11997697-Nitric Oxide,
pubmed-meshheading:11997697-Nitric Oxide Synthase,
pubmed-meshheading:11997697-Oxadiazoles,
pubmed-meshheading:11997697-Pressoreceptors,
pubmed-meshheading:11997697-Rats,
pubmed-meshheading:11997697-Rats, Sprague-Dawley,
pubmed-meshheading:11997697-Receptors, Metabotropic Glutamate,
pubmed-meshheading:11997697-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:11997697-Receptors, Serotonin,
pubmed-meshheading:11997697-Receptors, Serotonin, 5-HT3,
pubmed-meshheading:11997697-Reflex,
pubmed-meshheading:11997697-Serotonin,
pubmed-meshheading:11997697-Serotonin Receptor Agonists,
pubmed-meshheading:11997697-Solitary Nucleus,
pubmed-meshheading:11997697-Synaptic Transmission
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pubmed:year |
2002
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pubmed:articleTitle |
Glutamate and NO mediation of the pressor response to 5-HT3 receptor stimulation in the nucleus tractus solitarii.
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pubmed:affiliation |
INSERM U.288, CHU Pitié-Salpêtrière, 91 blvd de l'Hôpital, 75634 Paris Cedex 13, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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