Calcium dynamics and homeostasis in a mathematical model of the principal cell of the cortical collecting tubule.
Calcium dynamics and homeostasis in a mathematical model of the principal cell of the cortical collecting tubule.
复制标题
皮质集合管主细胞数学模型中的钙动力学和稳态。
DOI：
10.1085/jgp.107.2.207
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Stephenson,JL
中科院分区：
文献类型：
--
作者：
Tang,Y;Stephenson,JL
将钙（Ca）动力学纳入Strieter等人（1992 a. Am. 263：F1063-1075）。根据IP（3）-敏感钙通道的Othmer-Tang模型（1993，在生物模式形成的实验和理论进展中，295-319）对Ca组分建模。内质网膜上存在IP（3）敏感的Ca通道和ATP驱动的泵。钙沿着其电化学梯度被动地进入细胞。基底外侧膜上的钙泵和Na/Ca交换是胞浆钙排出的主要原因。Na/Ca交换也可以反向模式操作以将Ca转运到细胞中。细胞质Ca对顶端Na通道的调节作用是在实验数据表明顶端Na渗透性与细胞质Ca浓度成反比后建模的。在细胞内钙的变化所造成的减少氯化钠在浴和管腔的数值结果是类似的实验在Bourdeau和刘（1990年）。Am. 258：F1497-1503）。这种模拟和实验的匹配需要Na/Ca交换器和Ca调节的顶端Na渗透性的协同作用。在均质培养基中，当细胞外Na严重降低时，细胞质Ca变得振荡，如在培养的主细胞的实验中观察到的（Koster，H.，C.货车O和R。宾德尔斯1993. Kidney Int.43：828-836）。这种基本上病理性的情况出现是因为由无Na培养基引起的膜电位的超极化增加了Ca流入细胞，而Na/Ca交换器被低细胞外Na失活并且不再能够有效地将Ca移出细胞。胞内Ca总量的增加引起胞质和内质网之间的振荡Ca运动。在细胞外Ca严重变化的情况下，研究Ca稳态。由于细胞外Ca减少，如果Ca不调节顶端离子转运，则Ca调节大大受损。模拟表明，单独的Na/Ca交换器仅具有有限的调节能力。钙调节的顶端钠或钾渗透性是必不可少的皮质集合小管的主细胞胞质钙的调节。
Calcium (Ca) dynamics are incorporated into a mathematical model of the principal cell in the cortical collecting tubule developed earlier in Strieter et al. (1992a. Am. J Physiol. 263:F1063-1075). The Ca components are modeled after the Othmer-Tang model for IP(3)-sensitive calcium channels (1993, in Experimental and Theoretical Advances in Biological Pattern Formation, 295-319). There are IP(3)-sensitive Ca channels and ATP-driven pumps on the membrane of the endoplasmic reticulum. Calcium enters the cell passively down its electrochemical gradient. A Ca pump and Na/Ca exchange in the basolateral membrane are responsible for the extrusion of cytoplasmic calcium. Na/Ca exchange can also operate in reverse mode to transport Ca into the cell. Regulatory effects of cytoplasmic Ca on the apical Na channels are modeled after experimental data that indicate apical Na permeability varies inversely with cytoplasmic Ca concentration. Numerical results on changes in intracellular Ca caused by decreasing NaCl in the bath and the lumen are similar to those from experiments in Bourdeau and Lau (1990. Am. J Physiol. 258:F1497-1503). This match of simulation and experiment requires the synergistic action of the Na/Ca exchanger and the Ca regulated apical Na permeability. In a homogeneous medium, cytoplasmic Ca becomes oscillatory when extracellular Na is severely decreased, as observed in experiments of cultured principal cells (Koster, H., C. van Os and R. Bindels. 1993. Kidney Int.43:828-836). This essentially pathological situation arises because the hyperpolarization of membrane potential caused by Na-free medium increases Ca influx into the cell, while the Na/Ca exchanger is inactivated by the low extracellular Na and can no longer move Ca out of the cell effectively. The raising of the total amount of intracellular Ca induces oscillatory Ca movement between the cytoplasm and the endoplasmic reticulum. Ca homeostasis is investigated under the condition of severe extracellular Ca variations. As extracellular Ca is decreased, Ca regulation is greatly impaired if Ca does not regulate apical ionic transport. The simulations indicate that the Na/Ca exchanger alone has only limited regulatory capacity. The Ca regulated apical sodium or potassium permeability are essential for regulation of cytoplasmic Ca in the principal cell of the cortical collecting tubule.