RP58866对哺乳动物心室肌细胞跨膜钾电流的影响。
Effects of RP58866 on transmembrane K+ currents in mammalian ventricular myocytes.
作者信息
Yang B F, Li G R, Xu C Q, Nattel S
机构信息
Department of Pharmacology, Harbin Medical University, Harbin 150086, China.
出版信息
Zhongguo Yao Li Xue Bao. 1999 Nov;20(11):961-9.
AIM
To determine effects of RP58866 on inward rectifier K+ current (IKl), transient outward K+ current (Ito) and delayed outward rectifier K+ current (IK) in isolated cardiac myocytes.
METHODS
In isolated ventricular myocytes of guinea pig and dog, the effect of RP58866 on IKl, Ito, and IK were observed by the whole cell voltage-clamp technique.
RESULTS
RP58866 decreased IKl in a concentration-dependent manner, with an IC50 of (3.4 +/- 0.8) micromol.L-1 (n = 6) at -100 mV in guinea pig ventricular cells. In dog ventricular myocytes, RP58866 inhibited Ito with IC50 of (2.3 +/- 0.5) micromol.L-1 at +40 mV. In guinea pig ventricular cells, RP58866 at 100 micromol.L-1 decreased IK: IKstep by (58 +/- 13)% at +40 mV, and IKtail by (86 +/- 17)%, respectively. RP58866 inhibited IKstep with an IC50 of (7.5 +/- 0.8) micromol.L-1, and IKtail with an IC50 of (3.5 +/- 0.9) micromol.L-1. The envelope of tail analysis suggested that both IKr and IKs were inhibited.
CONCLUSION
RP58866 inhibits IKl, Ito, and IK in cardiac myocytes with a similar potency, and is not a specific IKl inhibitor.
目的
确定RP58866对分离的心肌细胞内向整流钾电流（IKl）、瞬时外向钾电流（Ito）和延迟外向整流钾电流（IK）的影响。
方法
采用全细胞膜片钳技术，观察RP58866对豚鼠和犬分离心室肌细胞IKl、Ito和IK的影响。
结果
RP58866以浓度依赖方式降低IKl，在豚鼠心室细胞-100 mV时IC50为（3.4±0.8）μmol·L-1（n = 6）。在犬心室肌细胞中，RP58866在+40 mV时抑制Ito，IC50为（2.3±0.5）μmol·L-1。在豚鼠心室细胞中，100 μmol·L-1的RP58866降低IK：在+40 mV时IKstep降低（58±13）%，IKtail降低（86±17）%。RP58866抑制IKstep的IC50为（7.5±0.8）μmol·L-1，抑制IKtail的IC50为（3.5±0.9）μmol·L-1。尾电流分析表明IKr和IKs均被抑制。
结论
RP58866以相似的效力抑制心肌细胞中的IKl、Ito和IK，不是特异性的IKl抑制剂。
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