Imaging of Ca〔2+〕 Release by Caffeine and 9-Methyl-7-bromoeudistomin D and the Associated Activation of Large Conductance Ca〔2+〕-Dependent K〔+〕 Channels in Urinary Bladder Smooth Muscle Calls of the Guinea Pig

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  • Ohi Yoshiaki
    Department of Molecular and Cellular Pharmacology, Faculty of Pharmaceutical Sciences, Nagoya City University
  • Atsuki Kaoru
    Department of Molecular and Cellular Pharmacology, Faculty of Pharmaceutical Sciences, Nagoya City University
  • Torii Yuichi
    Department of Molecular and Cellular Pharmacology, Faculty of Pharmaceutical Sciences, Nagoya City University
  • Ohizumi Yasushi
    Department of Pharmaceutical Molecular Biology, Graduate School of Pharmaceutical Sciences, Tohoku University
  • Watanabe Minoru
    Department of Molecular and Cellular Pharmacology, Faculty of Pharmaceutical Sciences, Nagoya City University
  • Imaizumi Yuji
    Department of Molecular and Cellular Pharmacology, Faculty of Pharmaceutical Sciences, Nagoya City University

書誌事項

タイトル別名
  • Imaging of Ca2+ Release by Caffeine and 9-Methyl-7-bromoeudistomin D and the Associated Activation of Large Conductance Ca2+-Dependent K+ Channels in Urinary Bladder Smooth Muscle Cells of the Guinea Pig.
  • Imaging of Ca 2 Release by Caffeine and 9 Methyl 7 bromoeudistomin D and the Associated Activation of Large Conductance Ca 2 Dependent K Channels in Urinary Bladder Smooth Muscle Calls of the Guinea Pig
  • Imaging of Ca2+ Release by Caffeine and 9-Methyl-7-bromoeudistornin D and the Associated Activation of Large Conductance Ca2+-Dependent K+ Channels in Urinary Bladder Smooth Muscle Cells of the Guinea Pig

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抄録

Ca2+ release by caffeine and 9-methyl-7-bromoeudistomin D (MBED) and the concomitant activation of large conductance Ca2+-dependent K+ (BK) channels were analyzed using confocal Ca2+ imaging and whole cell voltage-clamp methods in guinea pig urinary bladder smooth muscle cells. Puff application of 3 or 10 mM caffeine for several seconds (2 - 5 s) elicited a large increase in intracellular Ca2+ concentration ([Ca2+]i) and induced a phasic outward current at a holding potential of −40 mV. The phasic outward current was the summation of spontaneous transient outward currents (STOCs) due to marked activation of BK channels and was followed by a short cessation of STOCs. Although the increase in superficial [Ca2+]i by caffeine was faster than that in global [Ca2+]i, the peak [Ca2+]i was identical in these areas. Puff application of 100 μM MBED also markedly enhanced STOCs for a few seconds. This response to MBED was not observed when stored Ca2+ was depleted by caffeine. The increase in [Ca2+]i by MBED occurred mainly in superficial areas. Longer application of 100 μM MBED for 2 min did not induce significant global [Ca2+]i increase but decreased the amount of Ca2+ release and cell shortening during the subsequent application of 10 mM caffeine. These results indicate that short application of MBED releases Ca2+ preferentially from superficial storage sites, presumably due to its slow approach to deeper sites. MBED may be a good pharmacological tool to manipulate selectively the superficial Ca2+ stores related to STOCs.

収録刊行物

  • Jpn.J.Pharmacol.

    Jpn.J.Pharmacol. 85 (4), 382-390, 2001

    公益社団法人 日本薬理学会

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