A COMPARISON OF CALCIUM CURRENTS IN RAT AND GUINEA-PIG SINGLE VENTRICULAR CELLS
A COMPARISON OF CALCIUM CURRENTS IN RAT AND GUINEA-PIG SINGLE VENTRICULAR CELLS
复制标题
DOI：
10.1161/01.res.54.2.144
复制
发表时间：
1984-01-01
影响因子：
20.1
通讯作者：
BROWN, AM
中科院分区：
文献类型：
--
作者：
JOSEPHSON, IR;SANCHEZCHAPULA, J;BROWN, AM
使用酶解的单心室细胞比较大鼠和豚鼠心脏中缓慢的内向 Ca 电流。采用单电极电压钳，采用分时法分别对电流和电压进行采样。通过用相隔 50 μm 的 2 个微电极测量电势来评估峰值缓慢内向 Ca 电流期间膜电势的空间均匀性；电位彼此相差在 3 mV 以内。两个物种的缓慢内向 Ca 电流的峰值电流-电压关系相似，但与豚鼠相比，大鼠的各个电流显示出更快的失活时间过程和更慢的失活恢复时间过程。 K 电流阻滞剂 4-氨基吡啶和四乙基氯化铵对本研究中使用的保持电位（-50 至 -40 mV）记录的净膜电流没有产生显着影响。使用双脉冲程序探索了缓慢内向 Ca 电流失活的基本机制。使用双脉冲程序对大鼠和豚鼠心脏细胞的预脉冲进行了研究。在大鼠和豚鼠心脏细胞中，预脉冲到非常正的电位与随后的测试脉冲中缓慢的内向 Ca 电流的部分恢复相关。此外，内部乙二醇-双N,N,N'',N''-四乙酸或用Ba替代Ca可减缓大鼠心脏细胞中缓慢的内向Ca电流的失活速率。然而，由于去极化预脉冲对超极化测试脉冲缺乏影响，非特异性电流的 Ca 激活不太可能产生这些结果。失活的 Ca 依赖性成分可能是造成这些物种中缓慢内向 Ca 电流的失活和恢复时间过程中观察到的差异的原因。
The slow inward Ca currents were compared in rat and guinea pig heart using enzymatically dissociated, single ventricular cells. A single electrode voltage clamp was used, in which current and voltage were sampled separately using a time-sharing method. Spatial homogeneity of membrane potential during peak slow inward Ca current was assessed by measuring the potential with 2 microelectrodes 50 .mu.m apart; the potentials were within 3 mV of each other. Peak current-voltage relations for slow inward Ca currents were similar for the 2 species, but the individual currents showed a faster time course of inactivation and a slower time course of recovery from inactivation for rat, compared with guinea pig. The K current blockers 4-aminopyridine and tetraethylammonium chloride did not produce significant effects on the net membrane currents recorded at the holding potentials (-50 to -40 mV) used in this study. The underlying mechanism for the inactivation of the slow inward Ca currents was explored using a double pulse procedure. In both rat and guinea pig heart cells prepulses to was explosred using a double pulse procedure. In both rat and guinea pig heart cells prepulses to very positive potentials were associated with a partial restoration of the slow inward Ca current in the following test pulse. In addition, internal ethylene glycol-bis N,N,N'',N''-tetraacetic acid or substitution of Ba for Ca slowed the rate of inactivation of the slow inward Ca current in rat heart cells. Ca activation of nonspecific currents was though less likely to have produced these results due to the lack of effect of depolarizing prepulses on hyperpolarizing test pulses. A Ca-dependent component of inactivation may be responsible for the differences observed in both the inactivation and the recovery time courses of the slow inward Ca current in these species.