| Project/Area Number |
15580256
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Basic veterinary science/Basic zootechnical science
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| Research Institution | Gifu University |
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Principal Investigator |
TAKEWAKI Tadashi Gifu University, Applied biological science, Professor, 応用生物科学部, 教授 (00021717)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMIZU Yasutake Gifu University, Applied biological science, Associate Professor, 応用生物科学部, 助教授 (40243802)
KOMORI Seiichi Gifu University, Applied biological science, Professor, 応用生物科学部, 教授 (70195866)
UNNO Toshihiro Gifu University, Applied biological science, Associate Professor, 応用生物科学部, 助教授 (90252121)
ATOJI Yasuro Gifu University, Applied biological science, Professor, 応用生物科学部, 教授 (90151084)
MATSUYAMA Hayato Gifu University, Applied biological science, Research Associate, 応用生物科学部, 助手 (80345800)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2003: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | cerebral / electrical signal / transmitter / endothelium / vessel / basilar / ATP / serotonin / 脳血流 / アストロサイト / セロトニン / 一酸化窒素作動性神経 |
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| Research Abstract |
The mechanisms of spatial and electrical signaling were investigated by measuring the changes of membrane potentials or tone in the longitudinal and circular smooth muscle of the cerebral and mesenteric artery using electrophysiological and pharmacological technique. Electrical field stimulation evoked a fast and slow depolarization. This depolarization recorded from the chicken and hamster mesenteric artery Were tetrodototin-sensitive, and atropine/prazosin-insensitive. Atropine/prazosin-resistant component was blocked by the nonspecific purinergic antagonist, suramin, in a dose-dependent manner, indicating that this component is mediated by the neurotransmitter adenine 5'-triphosphate (ATP) from sympathetic nerve terminals innervating mesenteric arteries. On the other hand, depolarization's recorded from the hamster cerebral Artery was partially resistant after the administration of tetrodotoxin or calcium antagonists. Neither desensitization nor blocking of P2X receptor with its put
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ative receptor agonist alpha, meta-methylene ATP and its antagonist pyridoxalphosphate-6-azophenyl-2',4'-disulfonie, had significant effect on the purznergic depolarization. In contrast, either desensitization or blocking of P2Y receptor with its putative agonist 2-methylthioATP and its antagonist Cibacron blue abolished the purinergic depolarization, indicating that this response is mediated through P2Y but not P2X receptor. Neutrally released ATP elicited biphasic responses that were initially excitatory junction potentials followed by a sustaining depolarization in the smooth muscle of the cerebral artery. ATP induced the release of endothelium-derived hyperpolarizing factor from endothelial cells. The present findings demonstrated that ATP released from the sympathetic nerves diffuse as far as the endothelium and activate P2Y-loke receptors to induce the release of endothelium-derived hyperpolarizing factors in thin arteries, but not in thick arteries. Endothelium derived hyperpolarizating factors appears to be a primary functional factor in small peripheral artery, thus it's proposed that these factor released by neural ATP may play an important physiological role in the local regulation of vascular resistance. The purinergic depolarization was inhibited by pertussis toxin. Furthermore, it was significant inhibited by a phospholipase C inhibitor, indicating that the receptors involved in mediating the purinergic depolarization are linked to a pertussis toxin-sensitive G-protein. Hamster basilar arteries reconstructed by noradrenalin were relaxed by acetylcholine. The relaxation was reduced by N-nitro L-argentine (L-NA) and by indomethacin. L-NA significantly increased the muscle tone in non-contracted arteries, whereas indomethacin decreased it. In noradrenalin reconstructed arteries, serotonin induced at low concentration (1-10nM) a reduction in tone and induced an increase in tone at higher concentration Endothelial lesion increased about twofold the contraction of indomethacin^treated arteries to serotonin. It appears that serotonin causes the release from the endothelium of two vasoactive factors, one of which is probably the vasodilator nitric oxide ; second factor is a cyclooxygenase-dependent contractile substance. In mesenteric artery, electrical field stimulation-induced excitatory membrane response occurring in the smooth muscle is mainly purinergicin nature and is mediated via P2Y purinoceptors. Less
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