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目的为研究β3肾上腺素能受体介导的心脏生物学效应--β3肾上腺素能受体激活后心肌细胞电生理活动的变化。方法以原代培养的豚鼠心肌细胞为对象,采用全细胞膜片钳技术记录心肌细胞孵育β3肾上腺素能受体激动剂4-[-[2-hydroxy-(3-chlorophenyl)ethyl-amino]propyl]phenoxyacetate(BRL-37344;BRL)5～10min前后ICa-L,Ito(L型钙离子通道和瞬时外向钾通道)的变化。结果显示10-6mol/L的BRL显著增强豚鼠心肌细胞的Ito,上移I-V曲线;去极化刺激到+80mV时,电流密度从(6.11±1.03)pA/pF上升到(8.46±2.07)pA/pF(n=6,P=0.013064)。10-6mol/L的BRL显著增强豚鼠心肌细胞的ICa-L,为对照组的(2.30±0.75)倍(n=5,P=0.0063);去极化刺激到+10mV时,电流幅度从(89.25±17.83)pA上升到(205.00±72.24)pA。结论 BRL-37344可增强豚鼠心肌瞬时外向钾电流和L型钙电流,进而调控心脏的活动。
Aim To investigate the effects of β3 adrenergic receptor-mediated cardiac biology on the electrophysiological activity of cardiomyocytes after β3-adrenergic receptor activation. Methods Cardiomyocytes were incubated with primary cultured guinea pig cardiomyocytes for whole-cell patch clamp recording of β3-adrenergic receptor agonist 4 - [- [2-hydroxy- (3-chlorophenyl) ethyl- phenoxyacetate (BRL-37344; BRL) before and after 5 ~ 10min ICa-L, Ito (L-type calcium channel and transient outward potassium channels) changes. The results showed that 10-6mol / L BRL significantly increased Ito and IV curve of guinea pig cardiomyocytes, while the current density increased from (6.11 ± 1.03) pA / pF to (8.46 ± 2.07) pA when depolarization was stimulated to +80 mV /pF(n=6,P=0.013064). 10-6mol / L BRL significantly increased ICa-L of guinea pig cardiomyocytes (2.30 ± 0.75) times that of the control group (n = 5, P = 0.0063); when the depolarization was stimulated to +10 mV, 89.25 ± 17.83) pA increased to (205.00 ± 72.24) pA. Conclusion BRL-37344 can enhance the transient outward potassium current and L-type calcium current in guinea pig myocardium, and then regulate cardiac activity.