Effects of stress on the rapid component of delayed rectifier potassium current in rat cardiomyocytes
10.11855/j.issn.0577-7402.2017.08.06
- VernacularTitle:应激刺激对大鼠心肌细胞快激活延迟整流钾电流改变的影响
- Author:
Jiangli QI
;
Zhongqi CAI
;
Ying DONG
;
Yundai CHEN
;
Yang LI
;
Yanan XIE
;
Wang LI
;
Xuebin CAO
- Keywords:
stress;
arrhythmia;
IKr current;
patch clamp technique
- From:
Medical Journal of Chinese People's Liberation Army
2017;42(8):692-697
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of stress on the rapid component of delayed rectifier potassium current (IKr) in rat cardiomyocytes. Methods Forty male SD rats were randomly divided into four groups (10 each): control group (Ctrl), exhaustive group (ES), noise group (WN) and composite group (ES+WN). Stress animal models were prepared as follows: Rats in ES group were undergoing exhaustive swimming as the stress factor, in WN group undergoing white noise and in ES+WN group undergoing exhaustive swimming + white noise as the stress factor. Langendorff device was used to reversely perfuse collagenase for isolating the rat's ventricular myocytes. The effect of stress on IKr current and gating mechanism of single ventricular myocyte was recorded by whole-cell patch clamp technique. Results Compared with the Ctrl group, the tail current density of IKr (IKr,tail) of ventricular myocytes increased significantly in ES group and WN group (P<0.01). The IKr,tail current density of the ventricular myocytes in ES+WN group was significantly higher than that in ES group and WN group (P<0.01), and the effect was voltage dependent. Gating mechanism revealed that the half inactivation voltage of IKr,tail (V1/2,inact) can be shifted to the right in ES group, WN group and ES+WN group when compared with the Ctrl group, and the recovery time constant shortened after inactivation (P<0.01). However, the steady-state activation, fast inactivation constant and voltage dependence of IKr,tail were not statistically significant in ES group, WN group and ES+WN group when compared with the Ctrl group. Conclusion Stress increases the IKr current in rat cardiomyocytes, suggesting it be one of the electrophysiological bases of stress-induced arrhythmia.
