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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5 Pt 1
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pubmed:dateCreated |
1993-6-22
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pubmed:abstractText |
The mechanisms by which cAMP and cGMP and agents that stimulate one (isoproterenol and nitroprusside) or both cyclic nucleotides (VIP) decrease cytosolic free Ca2+ ([Ca2+]i) and inhibit contraction were examined in dispersed, intact, and saponin-permeabilized gastric muscle cells. In these cells, the [Ca2+]i transient responsible for initial contraction is mediated by inositol 1,4,5-trisphosphate (IP3)-dependent Ca2+ release (K. N. Bitar, P. G. Bradford, J. W. Putney, Jr., and G. M. Makhlouf, Science Wash. DC 232: 1143-1145, 1986, and J. Biol. Chem. 261: 16591-16596, 1986). In intact muscle cells, dibutyryl cAMP and all three relaxant agents inhibited contraction, [Ca2+]i, and net Ca2+ efflux (i.e., Ca2+ release) in a concentration-dependent fashion. In permeabilized muscle cells, cAMP, cGMP, and all three relaxant agents 1) inhibited cholecystokinin (CCK)-induced IP3 production (maximal 38-48%), 2) inhibited CCK- and IP3-induced Ca2+ efflux (maximal 55-59%) and contraction (maximal 59-66%), and 3) stimulated Ca2+ uptake (maximal 25-30%), in a concentration-dependent fashion. cAMP and cGMP were equipotent inhibitors of IP3 production and of CCK- and IP3-induced Ca2+ efflux and contraction, whereas cGMP was distinctly more potent as a stimulant of Ca2+ uptake. For all functions, maximal effects induced by cAMP and cGMP were similar to those induced by the three relaxant agents. Inhibition of Ca2+ release was the main determinant of inhibition of contraction; stimulation of Ca2+ uptake was relatively minor (< 5% of Ca2+ efflux). Decrease in IP3 production did not contribute to inhibition of Ca2+ efflux and contraction since inhibition of IP3-induced Ca2+ efflux was similar to inhibition of CCK-induced IP3-dependent Ca2+ efflux.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:grant | |
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,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Radioisotopes,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol,
http://linkedlifedata.com/resource/pubmed/chemical/Nitroprusside,
http://linkedlifedata.com/resource/pubmed/chemical/Sincalide,
http://linkedlifedata.com/resource/pubmed/chemical/Vasoactive Intestinal Peptide
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
264
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
G967-74
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8388644-Animals,
pubmed-meshheading:8388644-Calcium,
pubmed-meshheading:8388644-Calcium Radioisotopes,
pubmed-meshheading:8388644-Cyclic AMP,
pubmed-meshheading:8388644-Cyclic GMP,
pubmed-meshheading:8388644-Dose-Response Relationship, Drug,
pubmed-meshheading:8388644-Guinea Pigs,
pubmed-meshheading:8388644-Inositol 1,4,5-Trisphosphate,
pubmed-meshheading:8388644-Isoproterenol,
pubmed-meshheading:8388644-Kinetics,
pubmed-meshheading:8388644-Muscle, Smooth,
pubmed-meshheading:8388644-Muscle Contraction,
pubmed-meshheading:8388644-Muscle Relaxation,
pubmed-meshheading:8388644-Nitroprusside,
pubmed-meshheading:8388644-Sincalide,
pubmed-meshheading:8388644-Stomach,
pubmed-meshheading:8388644-Vasoactive Intestinal Peptide
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pubmed:year |
1993
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pubmed:articleTitle |
Inhibition of IP3 and IP3-dependent Ca2+ mobilization by cyclic nucleotides in isolated gastric muscle cells.
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pubmed:affiliation |
Department of Medicine, Medical College of Virginia, Richmond 23298.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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