Modulation of calcium channel currents in guinea‐pig single ventricular heart cells by the dihydropyridine Bay K 8644.
Modulation of calcium channel currents in guinea‐pig single ventricular heart cells by the dihydropyridine Bay K 8644.
复制标题
二氢吡啶 Bay K 8644 对豚鼠单心室心脏细胞钙通道电流的调节。
DOI：
--
复制
发表时间：
1988
期刊：
影响因子：
--
通讯作者：
B. Nilius
中科院分区：
文献类型：
--
作者：
F. Markwardt;B. Nilius
1.采用细胞内透析的单玻璃微管电压钳技术研究豚鼠心室肌细胞的Ba 2+电流。在37 ℃下评价了1，4-二氢吡啶Bay K 8644对全细胞电流的影响。2. Bay K 8644在-50 mV和+20 mV之间的测试电位下增加了Ba 2+峰电流，并使电流-电压关系向超极化电位方向移动（Ca 2+通道激活的电流-电压关系移动，13.8 +/-4.1 mV; n = 9; Bay K 8644，5 mumol/l）。3.在Bay K 8644后，在-40 mV和+20 mV之间的测试电压范围内，Ba 2+电流的峰值时间减少，同时根据记录的电流与d2 f模型的拟合估计的激活时间常数缩短。4. Ba ~（2+）电流的衰减用两个指数拟合，包括一个基座。化合物Bay K 8644在整个电压范围内加速了快速衰减。Ba 2+电流的快速失活成分的幅度显着增加后，应用Bay K 8644。5.使用0.5或5 s预脉冲的稳态失活向超极化电位偏移（电压偏移10.3 +/-5.2 mV; n = 4; Bay K 8644，5 mumol/l）。6. Bay K 8644修饰的Ba 2+电流的时程变化不能仅通过Ca 2+通道从开放状态到关闭状态的反向速率系数的降低来描述（Sanguinetti，Krafte & Kass，1986）。Bay K 8644对失活的影响可以通过电流依赖性失活模型（Standen &斯坦菲尔德，1982）定性和定量描述，假设内部结合位点对Ba 2+的亲和力低于对Ca 2+的亲和力。
1. A single glass micropipette voltage clamp technique with intracellular dialysis was used to study Ba2+ currents in isolated ventricular cells from guinea‐pig hearts. Effects of the 1,4‐dihydropyridine Bay K 8644 on whole‐cell currents were evaluated at 37 degrees C. 2. Bay K 8644 increased the Ba2+ peak currents at test potentials between ‐50 and +20 mV and shifted the current‐voltage relationships towards hyperpolarizing potentials (leftward shift for Ca2+ channel activation, 13.8 +/‐ 4.1 mV; n = 9; Bay K 8644, 5 mumol/l). 3. The peak times of the Ba2+ currents were diminished over the voltage range tested between ‐40 and +20 mV after Bay K 8644 in parallel with a shortening of the time constant of activation that was estimated from fits of the recorded currents with a d2f model. 4. The decay of the Ba2+ currents was fitted with two exponentials including a pedestal. The compound Bay K 8644 accelerated the fast decay over the whole voltage range. The amplitude of the rapidly inactivated component of the Ba2+ currents was strikingly increased after application of Bay K 8644. 5. The steady‐state inactivation using a 0.5 or 5 s pre‐pulse was shifted towards hyperpolarizing potentials (leftward shift 10.3 +/‐ 5.2 mV; n = 4; Bay K 8644, 5 mumol/l). 6. The change in the time course of Bay K 8644‐modified Ba2+ currents cannot be described solely by a decrease of the backward rate coefficient from an open to a closed state of the Ca2+ channel (Sanguinetti, Krafte & Kass, 1986). The described effects of Bay K 8644 on the inactivation can be both qualitatively and quantitatively described by a model of current‐dependent inactivation (Standen & Stanfield, 1982), assuming a lower affinity of an internal binding site for Ba2+ than for Ca2+.
新型 Ca2 激动剂 (Bay K 8644) 增强并诱导心脏慢动作电位。
DOI：
10.1152/ajpheart.1984.247.2.h337
发表时间：
1984
期刊：
The American journal of physiology
影响因子：
--
作者：
Wahler,GM;Sperelakis,N
通讯作者：
Sperelakis,N