Methyl-β-cyclodextrin prevents Ca2+-induced Ca2+ release in smooth muscle cells of mouse urinary bladder

Methyl-β-cyclodextrin prevents Ca2+-induced Ca2+ release in smooth muscle cells of mouse urinary bladder
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DOI:
10.1254/jphs.sc0060213
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发表时间:
2007-01-01
影响因子:
3.5
通讯作者:
Imaizumi, Yuji
Imaizumi, Yuji
中科院分区:
医学3区
文献类型:
--
作者:
Hotta, Shingo;Yamamura, Hisao;Imaizumi, Yuji

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本文研究了甲基-1,8-环糊精(MPCD)对小鼠膀胱平滑肌细胞(SMCs)钙诱导钙释放(CICR)的影响。电压钳下UBSMCs的短去极化在20 ms内通过CICR在离散的肌膜下区域引起几个局部Ca 2+瞬变(Ca 2+热点)。随后,Ca ~(2+)波向整个区域扩散。用10 mM M β CD预处理可显著减弱UBSMCs中的Ca 2+热点,并减少UBSM条中单次直接电脉冲刺激引起的收缩。M β CD可能通过减弱电压依赖性Ca 2+通道与Ca 2+热点区ryanodine受体之间的偶联来预防CICR。
We examined the effects of methyl-,8-cyclodextrin (MPCD) on Ca2+-induced Ca2+ release (CICR) in smooth muscle cells (SMCs) of mouse urinary bladder (UB). Short depolarization of UBSMCs under voltage-clamp elicited several local Ca2+ transients (Ca2+ hot spots) via CICR within 20 ms in discrete sub-sarcolemmal areas. Then, the Ca2+ wave spread to whole areas. The pretreatment with 10 mM M beta CD significantly attenuated Ca2+ hot spots in UBSMCs and reduced contraction by single direct electrical pulse stimulation in UBSM strips. M beta CD may prevent CICR by attenuating the coupling between voltage-dependent Ca2+ channels and ryanodine receptors in Ca2+ hot spot areas.