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平滑肌中机电偶联和药机偶联的不同收缩系统。

Distinct contractile systems for electromechanical and pharmacomechanical coupling in smooth muscle.

作者信息

Lamounier-Zepter Valéria, Baltas Leonidas G, Morano Ingo

机构信息

Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.

出版信息

Adv Exp Med Biol. 2003;538:417-25; discussion 425-6. doi: 10.1007/978-1-4419-9029-7_39.

Abstract

Electromechanical coupling by KCl depolarization of bladder preparations elicits an initial phasic and subsequent tonic contraction. Using a smooth-muscle myosin heavy chain (SM-MyHC) knock-out mouse model we could previously demonstrate, that phasic and tonic contraction of intact neonatal bladder preparations could be elicited through the recruitment of SM-MyHC and non-muscle myosin heavy chains (NM-MyHC), respectively. Inhibition of myosin light chain kinase (MLCK) by ML-7 eliminated the phasic contraction of wild-type (+/+), rather than tonic contraction of neonatal bladder strips prepared from both +/+ and homozygous SM-MyHC knock-out (-/-) mice. Pharmacomechanical coupling upon PDBu-induced activation of protein kinase C of neonatal bladder preparations elicited tonic contraction of both +/+ and -/- murine. We suggest that: i) electromechanical coupling activates both SM-MyHC and NM-MyHC systems via a ML-7 sensitive and insensitive pathway, respectively. ii) Pharmacomechanical coupling recruits part of the NM-MyHC system rather than SM-MyHC.

摘要

氯化钾使膀胱组织去极化引发的机电耦联会引起初始的相性收缩和随后的强直性收缩。利用平滑肌肌球蛋白重链(SM-MyHC)基因敲除小鼠模型,我们之前能够证明,完整新生膀胱组织的相性收缩和强直性收缩可分别通过募集SM-MyHC和非肌肉肌球蛋白重链(NM-MyHC)来引发。ML-7对肌球蛋白轻链激酶(MLCK)的抑制消除了野生型(+/+)小鼠的相性收缩,而不是消除了由+/+和纯合SM-MyHC基因敲除(-/-)小鼠制备的新生膀胱条带的强直性收缩。佛波酯(PDBu)诱导新生膀胱组织的蛋白激酶C激活后产生的药物机械耦联引发了+/+和-/-小鼠的强直性收缩。我们认为:i)机电耦联分别通过对ML-7敏感和不敏感的途径激活SM-MyHC和NM-MyHC系统。ii)药物机械耦联募集了部分NM-MyHC系统而非SM-MyHC。

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