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rdf:type |
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lifeskim:mentions |
umls-concept:C0034193,
umls-concept:C0205421,
umls-concept:C0439799,
umls-concept:C0439834,
umls-concept:C0442805,
umls-concept:C0449432,
umls-concept:C0678544,
umls-concept:C0999699,
umls-concept:C1179435,
umls-concept:C1314939,
umls-concept:C1524073,
umls-concept:C1548799,
umls-concept:C1705248
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pubmed:issue |
Pt 3
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pubmed:dateCreated |
2002-5-2
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pubmed:abstractText |
Regenerative potentials were initiated by depolarizing short segments of single bundles of circular muscle isolated from the gastric antrum of guinea-pigs. When changes in [Ca(2+)](i) and membrane potential were recorded simultaneously, regenerative potentials were found to be associated with an increase in [Ca(2+)](i), with the increase starting after a minimum latency of about 1 s. Although the increase in [Ca(2+)](i) was reduced by nifedipine, the amplitudes of the regenerative responses were little changed. Regenerative responses and associated changes in [Ca(2+)](i) were abolished by loading the preparations with the Ca(2+) chelator MAPTA-AM. Regenerative potentials were abolished by 2-aminoethoxydiphenyl borate (2APB), an inhibitor of IP(3) induced Ca(2+) release, by N-ethylamaleimide (NEM), an alkylating agent which blocks activation of G-proteins and were reduced in amplitude by two agents which block chloride (Cl(-))-selective channels in many tissues. The observations suggest that membrane depolarization triggers IP(3) formation. This causes Ca(2+) release from intracellular stores which activates Ca(2+)-dependent Cl(-) channels.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-10066926,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-10087337,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-10200429,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-10332102,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-10373707,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-10432354,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-10747196,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-10811729,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-10896724,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-11251061,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-11287348,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-11351026,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-11490316,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-11507167,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-11579153,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-11850506,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-11986385,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-1214223,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-1328618,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-1667799,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-1709786,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-2175348,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-6146716,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-7108787,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-7525895,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-7853230,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-8120825,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-8308733,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-8690216,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-8769982,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-9348075,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-9409486,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-9782170,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11986379-9852332
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
540
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
907-19
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:11986379-Animals,
pubmed-meshheading:11986379-Calcium Channels,
pubmed-meshheading:11986379-Calcium Signaling,
pubmed-meshheading:11986379-Chelating Agents,
pubmed-meshheading:11986379-Chloride Channels,
pubmed-meshheading:11986379-Egtazic Acid,
pubmed-meshheading:11986379-Guinea Pigs,
pubmed-meshheading:11986379-Membrane Potentials,
pubmed-meshheading:11986379-Muscle, Smooth,
pubmed-meshheading:11986379-Nifedipine,
pubmed-meshheading:11986379-Pyloric Antrum,
pubmed-meshheading:11986379-Reaction Time,
pubmed-meshheading:11986379-Regeneration
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pubmed:year |
2002
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pubmed:articleTitle |
Regenerative component of slow waves in the guinea-pig gastric antrum involves a delayed increase in [Ca(2+)](i) and Cl(-) channels.
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pubmed:affiliation |
Department of Zoology, University of Melbourne, Victoria 3010, Australia. d.hirst@zoology.unimelb.edu.au
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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