Effect of membrane potential on cytosolic calcium of bovine aortic endothelial cells.
Effect of membrane potential on cytosolic calcium of bovine aortic endothelial cells.
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膜电位对牛主动脉内皮细胞胞质钙的影响。
DOI：
10.1152/ajpheart.1989.257.3.h778
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Schilling,WP
中科院分区：
文献类型：
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作者：
Schilling,WP
通过测量亲脂性阳离子四[3 H]苯基磷（[3 H]TPP+）的摄取来评估缓激肽对培养的牛主动脉内皮细胞（BAECs）膜电位的影响。[3 H]TPP+的摄取被发现是1）细胞外K+浓度的函数，2）对缬氨霉素敏感，3）被K+通道抑制剂Ba 2+降低，这表明[3 H]TPP+的摄取响应于BAEC膜电位的变化。缓激肽（50 nM）在低K+缓冲液中产生的[3 H]TPP+摄取增加与缓激肽诱导的膜超极化一致。用高K+缓冲液膜去极化对缓激肽刺激的胞浆Ca 2+变化的影响使用荧光Ca 2+指示剂fura-2测定。这些实验的结果表明，无论是基础的胞质Ca 2+和缓激肽刺激释放的Ca 2+从内部存储不受膜去极化。然而，缓激肽刺激的Ca 2+从细胞外空间的流入减少与膜去极化的方式一致的运动的Ca 2+通过通道。
The effect of bradykinin on membrane potential of cultured bovine aortic endothelial cells (BAECs) was estimated by measuring the uptake of the lipophilic cation, tetra[3H]phenylphosphonium ([3H]TPP+). Uptake of [3H]TPP+ was found to be 1) a function of extracellular K+ concentration, 2) sensitive to valinomycin, and 3) decreased by the K+ channel inhibitor, Ba2+, suggesting that the uptake of [3H]TPP+ responds to changes in membrane potential of the BAEC. Bradykinin (50 nM) produced an increase in [3H]TPP+ uptake in low K+ buffer consistent with a bradykinin-induced membrane hyperpolarization. The effect of membrane depolarization with high K+ buffer on the bradykinin-stimulated changes in cytosolic Ca2+ was determined using the fluorescent Ca2+ indicator, fura-2. The results of these experiments demonstrated that both basal cytosolic Ca2+ and bradykinin-stimulated release of Ca2+ from internal stores were not affected by membrane depolarization. However, bradykinin-stimulated influx of Ca2+ from the extracellular space decreased with membrane depolarization in a manner consistent with the movement of Ca2+ through a channel.