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EXPRESSION OF IONIC CHANNELS DURING CARDIOVASCULAR DISEASE

EXPRESSION OF IONIC CHANNELS DURING CARDIOVASCULAR DISEASE
心血管疾病期间离子通道的表达
批准号:
10044313
负责人:
IMAIZUMI Yuji
金额:
$2.75万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B).
财政年份:
1998
资助国家:
日本
项目状态:
已结题
起止时间:
1998 至 1999

项目摘要

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IMAIZUMI Yuji的其他基金

相关文献

中文摘要
翻译
两个频道的离子电流密度之间的相互关系(voltage-dependent L-type Ca D12+ C1channels(VDCCs) and large conductance Ca D12+ C1activated C1D1 + C1channels(BKCs) and the mRNA expression level of their channel subtypes(R21c) was determined in rabbit smooth muscles。BK currents (I-D2K-Ca-D2) in the rabbit aorta were much smaller than those in the rabbit vas deferens。However, when CaイイD12+イエD1 current (IイD2 CaイエD2) was increased by Bay K8644, IイイD2K-CaイエD2 was also markedly increased especially in aortic smooth muscle cells。编码α1C中的mRNA内容的数量在初级bladder和vas中明显高于其在aorta和trachea中的含量。在对比中,编码两者的mRNA内容αBK和βBK在其四个问题中观察到类似水平。这些观察提高了VDCC和VDCC中定量差异的可能性 ... More BKC may provide an explanation for the differences in membrane excitability between aorta and trachea versus urinary bladder and vas deferens。The effects of ruthenium red (RuR) on contractility were examined in skinned fibers of guinea pig smooth muscles。Contractions of skinned fibers of the urinary bladder were enhManagement by RuR (EC-D250-D2=60-M)。pCa 6.0的接触增加到100μM RuR的320%。准确地说,相同的结果在线性长度光滑的Muscle layer和中间式Artery中获得。pCa 4.5诱导的最大接触在RuR中没有明显的影响。Application of microcystin, a potent protein phosphatase inhibitor, induced a tonic contraction of skinned smooth muscle at low [CaイイD12+イエD1] (pCa >8.0)。RuR对微细胞素诱导的契约有双重影响:低浓度的增强和高浓度的抑制。The relaxation following the decrease in [CaイD12+イエD1] from pCa 5. 0 to > 8. 0 was significantly slowed down by an addition of RuR.在pca6.3中的肌红蛋白光链磷酸化被RuR显著增加。These results indicate that RuR markedly increases CaイイD12+イエD1 sensitivity of the contractile system at least in part via inhibition of myosin light chain phosphatase。Spatiotemporal relationships between CaイD12+イエD1 sparks and the activation of transient ClイD1-イエD1 current were·zed in rabbit atrial myocytes based on simultaneous measurements of two dimensional CaイD12+ D1 images by fast scanning confocal microscopy and membrane currents under whole cell voltage-clamp。The results suggest that CaイイD12+イエD1 sparks initiate some patterns of global [CaイD12+イエD1]イイD2, and that either a CaイイD12+イエD1 hot spot or a CaイD12+イエD12+イエD1 wave is the spatiotemporal summation of individual CaイD12+イイD1 sparks, which results in the activation of CaイD12+イD1 dependent ion channels on the sarcolemma。It can be strongly suggested that a CaイイD12+イエD1 spark is a functional unit not only in excitation-contraction (E-C) coupling but also in the activation of CaイイD12+イエD1 dependent membrane current, mainly IイD2Cl-CaイエD2, in rabbit atrial myocytes。Less(低)
英文摘要
The interrelationship between the ionic current density of two channels (voltage-dependent L-type CaィイD12+ィエD1 channels (VDCCs) and large conductance CaィイD12+ィエD1 activated KィイD1+ィエD1 channels (BKCs) and the mRNA expression level of their channel subtypes (αィイD21cィエD2 subunit of L-type CaィイD12+ィエD1 channels (α1C) and α/β subunits of BK channel (αBK/βBK)) was determined in rabbit smooth muscles. BK currents (IィイD2K-CaィエD2) in the rabbit aorta were much smaller than those in the rabbit vas deferens. However, when CaィイD12+ィエD1 current (IィイD2CaィエD2) was increased by Bay K 8644, IィイD2K-CaィエD2 was also markedly increased especially in aortic smooth muscle cells. The amount of mRNA contents of encoding α1C was apparently higher in urinary bladder and vas deferens than that in aorta and trachea. In contrast, the mRNA contents of encoding both αBK and βBK were observed at similar levels in their four tissues. These observation raised the possibility that quantitative differences in the VDCC and … More BKC may provide an explanation for the differences in membrane excitability between aorta and trachea versus urinary bladder and vas deferens.The effects of ruthenium red (RuR) on contractility were examined in skinned fibers of guinea pig smooth muscles. Contractions of skinned fibers of the urinary bladder were enhanced by RuR (ECィイD250ィエD2=60μM). The contraction at pCa 6.0 was increased to 320% of control by 100μM RuR. Qualitatively the same results were obtained in the ileal longitudinal smooth muscle layer and mesenteric artery. Maximal contraction induced by pCa 4.5 was not affected significantly by RuR. Application of microcystin, a potent protein phosphatase inhibitor, induced a tonic contraction of skinned smooth muscle at low [CaィイD12+ィエD1] (pCa >8.0). RuR had a dual effect on the microcystin-induced contraction : enhancement at low concentrations and suppression at high concentrations. The relaxation following the decrease in [CaィイD12+ィエD1] from pCa 5.0 to >8.0 was significantly slowed down by an addition of RuR. Phosphorylation of myosin light chain at pCa 6.3 was significantly increased by RuR. These results indicate that RuR markedly increases CaィイD12+ィエD1 sensitivity of the contractile system at least in part via inhibition of myosin light chain phosphatase.Spatiotemporal relationships between CaィイD12+ィエD1 sparks and the activation of transient ClィイD1-ィエD1 current were analyzed in rabbit atrial myocytes based on simultaneous measurements of two dimensional CaィイD12+ィエD1 images by fast scanning confocal microscopy and membrane currents under whole cell voltage-clamp. The results suggest that CaィイD12+ィエD1 sparks initiate some patterns of global [CaィイD12+ィエD1]ィイD2iィエD2, and that either a CaィイD12+ィエD1 hot spot or a CaィイD12+ィエD1 wave is the spatiotemporal summation of individual CaィイD12+ィエD1 sparks, which results in the activation of CaィイD12+ィエD1 dependent ion channels on the sarcolemma. It can be strongly suggested that a CaィイD12+ィエD1 spark is a functional unit not only in excitation-contraction (E-C) coupling but also in the activation of CaィイD12+ィエD1 dependent membrane current, mainly IィイD2Cl-CaィエD2, in rabbit atrial myocytes. Less
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通讯作者:
Development of recombinant cell lines dying upon single action potentialoccurrence and the new screening system for compounds acting on ion channels
  • 批准号:
    23659046
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
  • 资助金额:
    $2.41万
  • 财政年份:
    2011
  • 负责人:
    IMAIZUMI Yuji
  • 依托单位:
Positive feedback mechanism for the regulation of intracellular Ca2+ concentration and related ion channels as novel drug targets
  • 批准号:
    23390020
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
  • 资助金额:
    $4.99万
  • 财政年份:
    2011
  • 负责人:
    IMAIZUMI Yuji
  • 依托单位:
Novel molecular functions of calcium-activated potassium channel as a target of drug development
  • 批准号:
    20390027
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
  • 资助金额:
    $12.65万
  • 财政年份:
    2008
  • 负责人:
    IMAIZUMI Yuji
  • 依托单位:
Analyses of calcium-activated potassium channels as novel targets for new drug therapy
  • 批准号:
    17390045
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
  • 资助金额:
    $10.3万
  • 财政年份:
    2005
  • 负责人:
    IMAIZUMI Yuji
  • 依托单位: