Regulation of single calcium channels in cerebral arteries by voltage, serotonin, and dihydropyridines.

Regulation of single calcium channels in cerebral arteries by voltage, serotonin, and dihydropyridines.
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通过电压、血清素和二氢吡啶调节脑动脉中的单个钙通道。

DOI:
10.1152/ajpheart.1991.261.6.h1951
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发表时间:
1991
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Nelson,MT
Nelson,MT
中科院分区:
--
文献类型:
--
作者:
Worley,JF;Quayle,JM;Standen,NB;Nelson,MT

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从兔脑(基底)动脉分离的平滑肌细胞上的细胞贴附贴片测量通过Ca通道的单位电流。钡(80和10 mM)和钙(80和10 mM)用作电荷载体。二氢吡啶Ca通道激动剂BAY R 5417用于增加开放状态概率(Popen),500 nM BAY R 5417在0 mV下使Popen增加10倍。在任何电压下,通过单个Ca通道的钡电流都大于钙电流,单通道电导负至-20 mV为24.6 pS(80 mM钡)、15.1 pS(80 mM钙)、17.2 pS(10 mM钡)和5.8 pS(10 mM钙)。每5 - 7 mV膜去极化(负至0 mV),单通道Popen增加2.7倍,在+0.4 mV(80 mM钙)和+13.5 mV(80 mM钡)时达到最大值的一半。具有钙但不具有钡作为电荷载体的Ca通道在-20 mV下表现出明显的正失活(半衰期,在0 mV下为112 ms)。二氢吡啶尼莫地平(2 nM)抑制通过Ca通道的平均电流。大脑动脉收缩剂5-羟色胺使单钙通道的Popen增加了200倍,而对单通道电导没有影响。经常观察到第二个明显的单一电流幅度,对应于约一半的更常见的水平的通道电导。小电导水平通道是电压依赖性的,不超过0.5秒的测试脉冲(钡),并可以激活5-羟色胺。
Unitary currents through Ca channels were measured from cell-attached patches on smooth muscle cells isolated from rabbit cerebral (basilar) arteries. Barium (80 and 10 mM) and calcium (80 and 10 mM) were used as the charge carriers. The dihydropyridine Ca channel agonist BAY R 5417 was used to increase open-state probability (Popen), with 500 nM BAY R 5417 increasing Popen 10-fold at 0 mV. Barium currents through single Ca channels were greater than calcium currents at any voltage, with single-channel conductances negative to -20 mV of 24.6 pS (80 mM barium), 15.1 pS (80 mM calcium), 17.2 pS (10 mM barium), and 5.8 pS (10 mM calcium). The single-channel Popen increased 2.7-fold per 5- to 7-mV membrane depolarization (negative to 0 mV) and was half maximal at +0.4 mV (80 mM calcium) and +13.5 mV (80 mM barium). Ca channels with calcium but not with barium as the charge carrier exhibited pronounced inactivation positive to -20 mV (half time, 112 ms at 0 mV). The dihydropyridine nimodipine (2 nM) inhibited average currents through Ca channels. The cerebral artery constrictor serotonin increased Popen of single Ca channels by as much as 200-fold without an effect on single-channel conductance. A second distinct amplitude of unitary currents was often observed, corresponding to a channel conductance of about one-half the more commonly observed level. The small-conductance-level channel was voltage dependent, did not inactivate over 0.5-s test pulses (with barium), and could be activated by serotonin.