Vasopressin stimulation of Ca2+ mobilization, two bivalent cation entry pathways and Ca2+ efflux in A7r5 rat smooth muscle cells.
Vasopressin stimulation of Ca2+ mobilization, two bivalent cation entry pathways and Ca2+ efflux in A7r5 rat smooth muscle cells.
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加压素刺激 A7r5 大鼠平滑肌细胞中的 Ca2 动员、两种二价阳离子进入途径和 Ca2 流出。
DOI：
10.1113/jphysiol.1995.sp020742
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
C. Taylor
中科院分区：
文献类型：
--
作者：
K. Byron;C. Taylor
1.用单细胞和群体方法研究了精氨酸加压素(AVP)对Fura-2负载的A7r5细胞钙转运的调节作用。2.AVP使细胞内游离钙浓度([Ca~(2+)]_i)呈浓度依赖性升高，达到一个不依赖于细胞外Ca~(2+)的峰值，并产生持续的Ca~(2+)信号，该信号是钙离子进入和流出之间平衡的结果。3.在无Ca~(2+)的培养液中，用thapsigargin、Ionomycin或预先用AVP处理耗尽细胞内的Ca~(2+)储备，可激活Ca~(2+)、Ba2+或Mn~(2+)的“容量性”进入。Ca~(2+)可抑制电容性Mn2+进入细胞内，而Sr2+和Ba2+都不能替代Ca~(2+)产生这种作用。4.在有空库的细胞中，AVP刺激进一步的二价阳离子进入，当细胞外Na+被N-甲基-D-葡萄糖胺取代或在去极化条件下(胞外KCl浓度([KCl]o)，135 mM)时，这种作用持续存在。因此，AVP的这种作用不仅仅是AVP引起膜超极化或刺激Na(+)-Ca~(2+)交换的结果，而是开放二价阳离子内流途径的结果。5.一些证据表明，AVP刺激的二价阳离子进入并不是细胞内存储更完全清空并导致电容途径进一步激活的结果。当细胞内的钙离子存储被离子霉素清空，并被thapsigargin阻止再填充时，AVP刺激Ba2+进入。Mn2+通过电容途径，但AVP不进一步增加Mn2+进入，证实AVP不进一步激活电容途径，两条途径对Mn2+的通透性不同。当细胞外[Sr2+]较低时，空库不会刺激可检测到的Sr2+进入，但AVP的加入会导致大量的Sr2+进入。6.在thapsigargin引起的[Ca~(2+)]_i持续升高过程中，加入50 nM AVP可引起[Ca~(2+)]_i下降。由于AVP不抑制电容通路，这一结果提示AVP刺激钙离子排出。7.我们认为AVP对A7r5细胞钙离子动员的刺激、二价阳离子进入的两种方式以及钙离子的外流都参与了A7r5细胞复杂的浓度依赖效应。
1. Arg8‐vasopressin (AVP)‐regulated Ca2+ transport were investigated in fura‐2‐loaded A7r5 cells using both single cell and population measurements. 2. AVP evokes an initial concentration‐dependent rise in cytosolic free Ca2+ concentration ([Ca2+ ]i) to a peak which is independent of extracellular Ca2+, and a sustained Ca2+ signal that results from a balance between stimulation of Ca2+ entry and efflux. 3. Depletion of intracellular Ca2+ stores with thapsigargin, ionomycin, or prior treatment with AVP in Ca2(+)‐free medium activates ‘capacitative’ entry of Ca2+, Ba2+ or Mn2+. Capacitative Mn2+ entry is inhibited by refilling stores with Ca2+; neither Sr2+ nor Ba2+ substitute for Ca2+ to give this effect. 4. In cells with empty stores, AVP stimulates further bivalent cation entry, and the effect persists when extracellular Na+ is replaced by N‐methyl‐D‐glucamine or under depolarizing condition (extracellular KCl concentration ([KCl]o), 135 mM). This effect of AVP is not therefore merely a consequence of AVP causing membrane hyperpolarization or stimulation of Na(+)‐Ca2+ exchange, but results from opening of a bivalent cation influx pathway. 5. Several lines of evidence indicate that AVP‐stimulated bivalent cation entry is not a consequence of more complete emptying of the intracellular stores and consequent further activation of the capacitative pathway. AVP stimulates Ba2+ entry when the intracellular Ca2+ stores have been both emptied by ionomycin and prevented from refilling by thapsigargin. Mn2+ permeates the capacitative pathway, but AVP does not further increase Mn2+ entry, confirming that AVP does not further activate the capacitative pathway and that the two pathways differ in their permeability to Mn2+. When the extracellular [Sr2+] is low, empty stores do not stimulate detectable Sr2+ entry, but addition of AVP causes substantial Sr2+ entry. 6. A decrease in [Ca2+]i occurs when 50 nM AVP is added during a sustained elevation of [Ca2+]i evoked by thapsigargin. Since AVP does not inhibit the capacitative pathway, this result suggests that AVP stimulates Ca2+ extrusion. 7. We conclude that stimulation of Ca2+ mobilization, two modes of bivalent cation entry, and Ca2+ efflux all contribute to the complex concentration‐dependent effects of AVP in A7r5 smooth muscle cells.
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影响因子：
4.8
作者：
M. Thibonnier;A. L. Bayer;M. Simonson;M. Kester
通讯作者：
M. Thibonnier;A. L. Bayer;M. Simonson;M. Kester
淋巴细胞质膜肌醇1,4,5-三磷酸受体：唾液酸的选择性富集和独特的结合特异性。
DOI：
10.1073/pnas.89.7.2849
发表时间：
1992
影响因子：
11.1
作者：
Khan,AA;Steiner,JP;Snyder,SH
通讯作者：
Snyder,SH
大鼠肝细胞中受体介导的 Ca2 信号传导机制。
DOI：
--
发表时间：
1991
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Hansen,CA;Yang,LJ;Williamson,JR
通讯作者：
Williamson,JR
影响因子：
4
作者：
PUTNEY, JW
通讯作者：
PUTNEY, JW