Drug-induced anomalous contraction of gastrointestinal tract of mice with impaired c-kit function.
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Accession number;04A0196241
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| Title;Drug-induced anomalous contraction of gastrointestinal tract of mice with impaired c-kit function. |
| Author;
TOKUTOMI NAOFUMI
(Kumamoto Univ., JPN)
TOKUTOMI YOSHIKO
(Kumamoto Univ., JPN)
NISHI KATSUHIDE
(Panapharm Lab. Co., Ltd., JPN)
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Journal Title;Folia Pharmacologica Japonica
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Journal Code:G0740A
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ISSN:0015-5691
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VOL.123;NO.3;PAGE.163-169(2004)
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| Figure&Table&Reference;FIG.5, REF.30 |
| Pub. Country;Japan |
| Language;Japanese |
| Abstract;Drug-induced contraction of gastrointestinal tracts seems to depend upon the extent of their rhythmic contraction that is driven by the activity of gastrointestinal pacemaker cells. In BALB/c mice chronically administrated with a neutralizing anti-c-Kit monoclonal antibody (ACK2), rhythmic contraction of the gastrointestinal tract was impaired and contractile responses to drugs, including acetylcholine, prostaglandin F2.ALPHA., and bradykinin, were anomalously augmented. Histochemical analysis of the c-kit-positive cells in the gastrointestinal tract revealed the decreased number of c-kit-positive cells in the ACK2-treated animals, which lead to the impaired rhythmic contraction. Since the intestinal c-kit-positive cells in primary culture developed Ca2+-dependent rhythmic Cl- current, the rhythmic current is supposed to be an origin of gastrointestinal pacemakers. The extent of anomaly in drug-induced contraction correlated with the extent of impairment in rhythmic contraction. The drug-induced anomalous contraction in the preparation from ACK2-treated animals, which is accompanied by the impaired rhythmic contraction, was mimicked when the gastrointestinal segments from control animals were superfused with a low temperature organ bath solution at 25.DEG.C.. These results suggest that rhythmic discharge of excitation of smooth muscle cells, which is triggered by rhythmic excitatory input from c-kit cells, regulates the extent of drug-induced contraction. (author abst.) |
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