1994 Fiscal Year Final Research Report Summary
The reaction to thromboxane thromboxane A_2 in smooth muscle cells
| Project/Area Number |
04670568
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | University of Occupational and Environmental Health, school of Medical Technology (1994)
University of Occupational and Environmental Health, Japan (1992-1993) |
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Principal Investigator |
TAKAHARA Kazuo University of Occupational and Environmental Helth, school of Medical Technology Associate Proffesor, 助教授 (30163306)
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| Co-Investigator(Kenkyū-buntansha) |
MIURA Yasushi University of Occupational and Environmental Helth, school of Medical Technology, 医療技術短期大学, 助手 (40270095)
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| Project Period (FY) |
1992 – 1994
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| Keywords | thromboxane A_2 / smooth muscle cell / platelets / calcium |
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| Research Abstract |
To study the reaction thromboxane A_2 in smooth muscle cells, we studied the reaction to thromboxane A_2 in platelets. The regulation of extracelluler Ca^<2+> entry into platelets was studied using nisoldipine. Nisoldipine or vehicle was added to fura2-loaded-platelets in the presence of CaCl_2 and an activator, a thromboxane A_2 agonist (U46619) or thrombin, was also added. In the other experiments, CaCl_2 was added after the activator to platelet samples containing EDTA.The U46619-evoked increase of [Ca^<2+>] i was suppressed by nisoldipine, but the thrombin-evoked [Ca^<2+>] i increase was not suppressed. When CaCl_2 was added to Ca^<2+>-free medium after platelet the activation, the increase of [Ca^<2+>] i due to U46619 was suppressed by nisoldipine, but not that due to thrombin. In addition, nisoldipine significantly suppressed platelet aggregation and secretion induced by U46619, but had no effect on the response to thrombin. These data suggest that Ca^<2+> entry through the platelet membrane is regulated by two or more types of Ca^<2+> channeles, including thromboxane A_2-activated and thrombin-activated channels. Only the former type of channel was blocked by nisoldipine.
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