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SMAKing Ca~(2+) sparks in arterial myocytes

机译:在动脉心肌细胞中产生Ca〜(2+)火花

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In the current issue of The Journal of Physiology, Essin et al. (2007) examined the relationship between Cavl.2 L-type Ca~(2+) channel function and Ca~(2+) spark activity in arterial myocytes. To do this, they took advantage of the SMAKO mouse (Moosmang et al. 2003) - a conditional, vascular smooth muscle-specific Cavl.2 knock-out mouse. Using SMAKO mice they provide what represents the strongest, most direct demonstration that, in arterial myocytes, local Ca~(2+) signalling between Cavl.2 channels and ryanodine receptors (RyRs) is not required for the activation of Ca~(2+) sparks. Rather, Cavl.2 activity influences Ca~(2+) spark activity in a subtler, indirect way by controlling sarcoplasmic reticulum (SR) Ca~(2+) load. The functional implications of these findings are discussed below
机译:在当前的《生理学杂志》中,Essin等人。 (2007)研究了Cavl.2 L型Ca〜(2+)通道功能与动脉心肌细胞Ca〜(2+)火花活性之间的关系。为此,他们利用了SMAKO小鼠(Moosmang等人,2003年)-一种有条件的血管平滑肌特异性Cav1.2敲除小鼠。他们使用SMAKO小鼠提供了最有力,最直接的证据,即在动脉心肌细胞中,激活Ca〜(2+)并不需要Cavl.2通道与ryanodine受体(RyRs)之间的局部Ca〜(2+)信号传导。 )火花。而是,Cavl.2活性通过控制肌浆网(SR)Ca〜(2+)负载以一种间接的方式影响Ca〜(2+)火花活性。这些发现的功能含义在下面讨论

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