Medicolegal study on alcohol-induced sudden death.(Effect of ethanol on vascular responses)
| Project/Area Number |
08457149
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Legal medicine
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| Research Institution | Nara Medical University |
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Principal Investigator |
HATAKE Katsuhiko Nara Medical University, DEPARTMENT ; Legal Medicine, professor, 医学部, 教授 (40164842)
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| Co-Investigator(Kenkyū-buntansha) |
MASUDA Chieko Nara Medical University, DEPARTMENT ; Legal Medicine, assistant, 医学部, 助手 (20264848)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥5,700,000 (Direct Cost: ¥5,700,000)
Fiscal Year 1997: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1996: ¥5,300,000 (Direct Cost: ¥5,300,000)
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| Keywords | Endothelium / EDRF / EDHF / superior mesenteric artery / rat |
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| Research Abstract |
Endothelial cells can produce and/or release not only endothelium-dereved relaxing factor (EDRF), identified as nitric oxide (NO), but also endothelium-hyperpolarizing factor (EDHF) which can hyperpolarize smooth muscle cells. EDRF activates guanylate cyclase and increases GMP in cyclic in smooth muscle cells, leading to relaxation of smooth muscles.
Ethanol is known to depress the relaxation response mediated by EDRF.However, there is no report as to whether ethanol can depress the relaxation response mediated by EDHF,which is not identified as yet. Therefore, we investigated the effect of ethanol on EDHF-mediated relaxation response using isolated rat superior mesenteric artery. Acetylcholine produced relaxation response in the presence of endothelium. The relaxation responses were partially depressed by NO inhibitor, N^G-nitro-L-arginine (L-NNA). The L-NNA resistant relaxations were abolished by 20 mM KCl and Ca^<++>-activated K channel inhibitors, tetraethylammonium and 4 aminopyridine but not ATP-sensitive K channel inhibitor, glibenclamide. Thus, the resistant relaxations were considered to be mediated by EDHF,which opens Ca-activated K channels. EtOH also depressed the L-NNA-resistant relaxations but not the relaxations induced by sodium nitroprusside. These results suggest that ethanol can depress the relaxations induced by both EDHF and EDRF and that the inhibitory mechanism is not non-specific action on smooth muscle cells. Although the inhibitory mechanisms of ethanol on EDHF-mediated relaxations is probably considered to occur at the level of endothelial cells further study is required to clarify the mechanisms.
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Report
(3 results)
Research Products
(4 results)
