1993 Fiscal Year Final Research Report Summary
The role of plasmalemmal Ca^<2+> channels and intracellular Ca^<2+> stores in vascular smooth muscles during the development of vascular resistance
Project/Area Number |
04660325
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
基礎獣医学
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Research Institution | Miyazaki University |
Principal Investigator |
ITO Katsuaki Miyazaki University, Faculty of Agriculture, Professor, 農学部, 教授 (70136795)
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Project Period (FY) |
1992 – 1993
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Keywords | Resistance vessels / Ca channels / Sarcoplasmic reticulum / Contraction / Intracellular Ca / Contractile protein / Phosphorylation / Membrane potential |
Research Abstract |
In this study, the roles of plasmalemmal Ca^<2+> channels and sarcoplasmic reticulum (SR), intracellular Ca^<2+> stores, in the development of tension in vascular smooth muscle, especially in resistance vessels, were investigated. The major findings are as follws. 1) Regulation of cytoplasmic Ca^<2+> ([Ca^<2+>]i) by Ca^<2+> channel and SR.I analyzed the effects of ryanodine and cyclopiazonic acid, modifiers of SR functions, on [Ca^<2+>]i, mesured with fura-2, and the tension of rat mesenteric resistance arteries. The results suggest that SR plays as a buffer to decrease [Ca^<2+>]i at a resting state, while it amplifies a contraction by releasing Ca^<2+> when transmembrane Ca^<2+> influx increased. 2) Ca^<2+> entry pathways following activation of alpha1-adrenoceptor. When alpha1-adrenoceptors of resistance vassels was activated by low concentration of agonist, Ca^<2+> influx through voltage-dependent Ca^<2+> channel (VDC) was enhanced without any depolarization. This influx triggered Ca^<2+> release from SR.A high concentration of agonist caused depolarization, which in turn enhanced the Ca^<2+> influx through VDC.Besides this, Ca^<2+> entry through a pathway other than VDC also occurred. This entry was sensitive to K^+ channel blockers but not to dihydropyridine Ca^<2+> channel blockers. 3) Functions of ion channels in the hypertensive vessels. In vascular smooth muscles from spontaneously hypertensive rate voltage-dependent Ca^<2+> channels were active at the resting state, which produced an active tension and activated Ca^<2+>-activated K^+ channels. Increased Ca^<2+> influx provided more Ca^<2+> to SR, then increased Ca^<2+> release from SR.
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Research Products
(10 results)
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[Publications] Asano,M.,Masuzawa-Ito,K.,Matsuda,T.,Imaizumi,Y.,Watanabe,M.& Ito,K.: "Functional role of Ca^<2+>-activated K^+ channels in resting state of carotid arteries from SHR" Am.J.Physiol.265. H843-H851 (1993)
Description
「研究成果報告書概要(和文)」より
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[Publications] Asano, M., Masuzawa-Ito, K., Matsuda, T., Imaizumi, Y., Watanabe, M.&Ito, K.: "Functional role of Ca^<2+>-activated K^+ channels in resting state of carotid arteries from SHR." American Journal Physiology. 265. H843-H851 (1993)
Description
「研究成果報告書概要(欧文)」より
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