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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-3
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pubmed:dateCreated |
1994-8-8
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pubmed:abstractText |
We used an electrophysiological approach (single sucrose gap) to compare the mechanism of action of selective tachykinin NK1 and NK2 receptor agonists ([Sar9]substance P sulfone and [beta ala8]neurokinin A-(4-10), respectively) in producing contraction of the circular muscle of the guinea-pig proximal colon. [Sar9]Substance P sulfone produced a marked depolarization, action potentials and increase in membrane conductance. On the other hand, [beta Ala8]neurokinin A-(4-10) produced less depolarization of the cell membrane and did not change membrane resistance. Nifedipine (1 microM) greatly reduced (80% inhibition) the contraction due to [Sar9]substance P sulfone while that due to [beta Ala8]neurokinin A-(4-10) was slightly affected (13% inhibition). Action potentials induced by either agonist were suppressed by nifedipine, while depolarization was reduced only to a minor extent. When tested in a Ca(2+)-free medium, the contraction produced by either agonist was greatly reduced (84-89%) as compared to the control. In organ bath experiments [Sar9]substance P sulfone and [beta Ala8]neurokinin A-(4-10) produced concentration-dependent contraction of the circular muscle of the colon (EC50 8 and 12 nM, respectively). Nifedipine (1 microM) markedly suppressed the response to [Sar9]substance P sulfone while that to [beta Ala8]neurokinin A-(4-10) was only slightly depressed. These findings demonstrate that NK1 receptor-mediated contraction is strictly linked to membrane depolarization and action potentials generation through nifedipine-sensitive Ca2+ channels (electromechanical coupling) while the NK2 receptor-mediated contraction is substantially unrelated to depolarization and, while being largely dependent upon extracellular Ca2+, is nifedipine-resistant, possibly linked to the opening of non-selective (Ca(2+)-permeable) receptor-gated cation channels (pharmacomechanical coupling).
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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 Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Neurokinin A,
http://linkedlifedata.com/resource/pubmed/chemical/Nifedipine,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Neurokinin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Neurokinin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tachykinin,
http://linkedlifedata.com/resource/pubmed/chemical/Substance P,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfones,
http://linkedlifedata.com/resource/pubmed/chemical/neurokinin A (4-10), beta-Ala(8)-,
http://linkedlifedata.com/resource/pubmed/chemical/substance P, Sar(9)-Met(O2)(11)-
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0014-2999
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
255
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
9-15
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7517885-Action Potentials,
pubmed-meshheading:7517885-Animals,
pubmed-meshheading:7517885-Calcium Channels,
pubmed-meshheading:7517885-Colon,
pubmed-meshheading:7517885-Electrophysiology,
pubmed-meshheading:7517885-Guinea Pigs,
pubmed-meshheading:7517885-Male,
pubmed-meshheading:7517885-Muscle, Smooth,
pubmed-meshheading:7517885-Muscle Contraction,
pubmed-meshheading:7517885-Neurokinin A,
pubmed-meshheading:7517885-Nifedipine,
pubmed-meshheading:7517885-Peptide Fragments,
pubmed-meshheading:7517885-Receptors, Neurokinin-1,
pubmed-meshheading:7517885-Receptors, Neurokinin-2,
pubmed-meshheading:7517885-Receptors, Tachykinin,
pubmed-meshheading:7517885-Substance P,
pubmed-meshheading:7517885-Sulfones
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pubmed:year |
1994
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pubmed:articleTitle |
Different Ca2+ influx pathways mediate tachykinin receptor-induced contraction in circular muscle of guinea-pig colon.
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pubmed:affiliation |
Department of Neuro-muscular Physiology, Bogomoletz Institute of Physiology, Kiev, Ukraine.
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pubmed:publicationType |
Journal Article,
In Vitro
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