| Project/Area Number |
04671360
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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 |
Biological pharmacy
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| Research Institution | Uuniversity of Shizuoka |
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Principal Investigator |
NAKAYAMA Koichi University of Shizuoka, Pharmaceutical Sciences, Professor, 薬学部, 教授 (50112769)
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| Co-Investigator(Kenkyū-buntansha) |
ISHII Kunio University of Shizuoka, Pharmaceutical Sciences, Assistant Professor, 薬学部, 助教授 (90137993)
TASNAKA Yoshio University of Shizuoka, Pharmaceutical Sciences, Assistant Professor, 薬学部, 助手 (60188349)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1992: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Cerebral and Coronary Artery / Biomechanics / Stretch / Stretch Activation / Mechanical Receptor / Vascontraction / Phopspholipase C / Ca^<2+> Signaling / 物理情報 / 圧負荷 / 筋原性収縮反応 / アーテリオグラフ / モノクロタリン肺高血圧 / Ca^<2+>チャネル |
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| Research Abstract |
Cerebral and coronary arteries are extremely sensitive to hemodynamic factors, i.e., biomichacal stimule, including blood pressure and blood flow. I have investigated the ca^<2+>-signaling mechanisms of mechanical reception in the cardiovascular system from the following point of view, and as a leader i have promoted the progress of this relatively underdeveloped research field. I have regarded the myogenic contractile reaction of blood vessels in response to stretch of vascular wall or an increase in intraluminal pressure as a kind of cellular/intracellular and Ca^<2+> signaling ; and 3) the cross-bridge property of contractile elements. I could have showed interesting results as follows which will promise the future progress in the research. I have found that membrane fluidity strongly affects the sensitivity of a mechano-receptor site, and an amiloride-sensitive component, a possible stretch-activated channel, may play a role in the genesis of myogenic activity. In addition, the biomechanical stimulus augmented the activity of phospholipase C, production of inositol trisphosphate, and increase in cytosolic Ca^<2+> concentration, which indicates a possible role of GTP-binging proteins coupled with this enxyme in the transformation of mechanical stimulus to cellular signalings. Moreover, myogenic activity is found to be in-between the contraction produced by phorbol esters and high K^+ depolarizing stimulus in the property of cross-bridge cycling. These results suggest that vascular reaction in response to biomechanical stimuli is mediated through a novel mechanisum of cellular signaling.
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