Kamp T J, Miller R J, Sanguinetti M C
Br J Pharmacol. 1985 Jun;85(2):523-8. doi: 10.1111/j.1476-5381.1985.tb08889.x.
Calcium (Ca2+)-dependent action potentials were recorded from 22 mM potassium (K+)-depolarized guinea-pig papillary muscle at several different pacing frequencies in the absence and presence of CGP 28 392 (10 microM), a Ca2+ channel agonist. The maximum upstroke velocity (Vmax) of the slow response action potential was measured to determine relative changes in Ca2+ current as a function of pacing frequency. CGP 28 392 increased Vmax more than two fold at low rates of stimulation (1 or 12 pulses min-1), but had no significant effect on Vmax during rapid pulsing (200 pulses min-1). The enhancement of Vmax was dependent upon extracellular [K+]. Increasing extracellular [K+] from 22 mM to 27 mM suppressed the frequency-dependent agonist effects and increased the antagonist effects on Vmax. These results indicate that CGP 28 392 is a partial Ca2+-channel agonist and suggest that its effects on Ca2+ current are voltage-dependent.
在不存在和存在Ca2+通道激动剂CGP 28 392（10微摩尔）的情况下，在几个不同的起搏频率下，从22毫摩尔钾（K+）去极化的豚鼠乳头肌记录钙（Ca2+）依赖性动作电位。测量慢反应动作电位的最大上升速度（Vmax），以确定作为起搏频率函数的Ca2+电流的相对变化。在低刺激频率（1或12次脉冲/分钟）下，CGP 28 392使Vmax增加两倍以上，但在快速脉冲（200次脉冲/分钟）期间对Vmax没有显著影响。Vmax的增强取决于细胞外[K+]。将细胞外[K+]从22毫摩尔增加到27毫摩尔可抑制频率依赖性激动剂效应，并增加对Vmax的拮抗剂效应。这些结果表明CGP 28 392是一种部分Ca2+通道激动剂，并表明其对Ca2+电流的影响是电压依赖性的。
