@article{JTD3615,
author = {Sen Wang and Xiao-Yan Min and Si-Si Pang and Jin Qian and Di Xu and Yan Guo},
title = {Adrenergic regulation of the rapid component of delayed rectifier K+ currents in guinea pig cardiomyocytes},
journal = {Journal of Thoracic Disease},
volume = {6},
number = {12},
year = {2014},
keywords = {},
abstract = {Background: Guinea pig ventricular cardiomyocytes display the rapid component of the delayed rectifier potassium current (Ikr) that contributes to ventricular repolarization and promotes stress-induced arrhythmias. Adrenergic stimulation favors ventricular arrhythmogenesis but its effects on Ikr are poorly understood.
Methods: Adrenergic modulation of Ikr was studied in isolated guinea pig ventricular cardiomyocytes using whole-cell patch clamping.
Results: We found that the Ikr amplitude was reduced to 0.66±0.02 and 0.62±0.03 in response to 0.1 μM phenylephrine (PE), an α1AR agonist, and 10 μM isoproterenol (ISO), a βAR agonist, respectively. The effect of PE can be blocked by the selective α1A-adrenoceptor antagonist 5-methylurapidil, but not by the α1Badrenoceptor antagonist chloroethylclonidine or α1D-adrenoceptor antagonist BMY7378. Additionally, the effect of ISO can be blocked by the β1-selective AR antagonist CGP-20712A, but not by the β2-selective AR antagonist ICI-118551. Although PE and ISO was continuously added to cells, ISO did not decrease the current to a greater extent when cells were first given PE. In addition, PE’s effect on Ikr was suppressed by β1AR stimulation.
Conclusions: Ikr can by regulated by both the α1 and β ARs system, and that in addition to direct regulation by each receptor system, crosstalk may exist between the two systems.},
issn = {2077-6624}, url = {https://jtd.amegroups.org/article/view/3615}
}