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首页> 外文期刊>American Journal of Physiology >Modulation of BK channel calcium affinity by differential phosphorylation in developing ovine basilar artery myocytes.
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Modulation of BK channel calcium affinity by differential phosphorylation in developing ovine basilar artery myocytes.

机译：在发育中的绵羊基底动脉肌细胞中通过差异磷酸化来调节BK通道钙亲和力。

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摘要

Large-conductance Ca2+-sensitive K+ (BK) channel activity is greater in basilar artery smooth muscle cells (SMCs) of the fetus than the adult, and this increased activity is associated with a lower BK channel Ca2+ set point (Ca0). Associated PKG activity is three times greater in BK channels from fetal than adult myocytes, whereas associated PKA activity is three times greater in channels from adult than fetal myocytes. We hypothesized that the change in Ca0 during development results from different levels of channel phosphorylation. In inside-out membrane patch preparations of basilar artery SMCs from adult and fetal sheep, we measured BK channel activity in four states of phosphorylation: native, dephosphorylated, PKA phosphorylated, and PKG phosphorylated. BK channels from adult and fetus exhibited similar voltage-activation curves, Ca0 values, and Ca2+ dissociation constants (Kd) for the dephosphorylated, PKA phosphorylated, and PKG phosphorylated states. However, voltage-activation curves of native fetal BK channels shifted significantly to the left of those of the adult, with Ca0 and Kd values half those of the adult. For the two age groups at each of the phosphorylation states, Ca0 and Kd produced linear relations when plotted against voltage at half-maximal channel activation. We conclude that the Ca0 and Kd values of the BK channel can be modulated by differential channel phosphorylation. Lower Ca0 and Kd values in BK channels of fetal myocytes can be explained by a greater extent of channel phosphorylation of fetal than adult myocytes.
机译：胎儿的基底动脉平滑肌细胞（SMC）中的大电导Ca2 +敏感K +（BK）通道活性比成人大，并且这种增加的活性与较低的BK通道Ca2 +设定点（Ca0）相关。在胎儿的BK通道中，相关的PKG活性是成年心肌细胞的三倍，而在成年人的BK通道中，相关的PKA活性是胎儿的心肌细胞的三倍。我们假设在发育过程中Ca0的变化是由不同水平的通道磷酸化引起的。在成年和胎羊基底动脉SMC的由内而外的膜片制剂中，我们测量了磷酸化四个状态下的BK通道活性：天然，去磷酸化，PKA磷酸化和PKG磷酸化。成人和胎儿的BK通道在去磷酸化，PKA磷酸化和PKG磷酸化状态下显示出相似的电压激活曲线，Ca0值和Ca2 +解离常数（Kd）。然而，天然胎儿BK通道的电压激活曲线明显向成年人的左侧移动，其中Ca0和Kd值为成年人的一半。对于在每个磷酸化状态下的两个年龄组，当对半最大通道激活时的电压作图时，Ca0和Kd产生线性关系。我们得出结论，BK通道的Ca0和Kd值可以通过差分通道磷酸化来调节。胎儿心肌细胞BK通道中Ca0和Kd值较低的原因是胎儿的通道磷酸化程度比成年心肌细胞更大。

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