甲基-β-环糊精可防止小鼠膀胱平滑肌细胞中钙离子诱导的钙离子释放。
Methyl-beta-cyclodextrin prevents Ca2+-induced Ca2+ release in smooth muscle cells of mouse urinary bladder.
作者信息
Hotta Shingo, Yamamura Hisao, Ohya Susumu, Imaizumi Yuji
机构信息
Department of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Japan.
出版信息
J Pharmacol Sci. 2007 Jan;103(1):121-6. doi: 10.1254/jphs.sc0060213. Epub 2007 Jan 1.
We examined the effects of methyl-beta-cyclodextrin (MbetaCD) on Ca(2+)-induced Ca(2+) release (CICR) in smooth muscle cells (SMCs) of mouse urinary bladder (UB). Short depolarization of UBSMCs under voltage-clamp elicited several local Ca(2+) transients (Ca(2+) hot spots) via CICR within 20 ms in discrete sub-sarcolemmal areas. Then, the Ca(2+) wave spread to whole areas. The pretreatment with 10 mM MbetaCD significantly attenuated Ca(2+) hot spots in UBSMCs and reduced contraction by single direct electrical pulse stimulation in UBSM strips. MbetaCD may prevent CICR by attenuating the coupling between voltage-dependent Ca(2+) channels and ryanodine receptors in Ca(2+) hot spot areas.
我们研究了甲基-β-环糊精（MβCD）对小鼠膀胱（UB）平滑肌细胞（SMC）中钙诱导钙释放（CICR）的影响。在电压钳制下，UB SMC的短暂去极化在离散的肌膜下区域内20毫秒内通过CICR引发了几个局部钙瞬变（钙热点）。然后，钙波扩散到整个区域。用10 mM MβCD预处理可显著减弱UB SMC中的钙热点，并减少UB SMC条带中单次直接电脉冲刺激引起的收缩。MβCD可能通过减弱钙热点区域中电压依赖性钙通道与ryanodine受体之间的偶联来阻止CICR。
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