ABSTRACT
Qiliqiangxin, a Chinese herb, represents the affection in Ca channel function of cardiac myocytes. It is unknown whether Qiliqiangxin has an effect on Na current and K current because the pharmacological actions of this herb's compound are very complex. We investigated the rational usage of Qiliqiangxin on cardiac ventricular myocytes of rats. Ventricular myocytes were exposed acutely to 1, 10, and 50 mg/L Qiliqiangxin, and whole cell patch-clamp technique was used to study the acute effects of Qiliqiangxin on Sodium current (I Na), outward currents delayed rectifier outward K(+) current (I K), slowly activating delayed rectifier outward K(+) current (I Ks), transient outward K(+) current (I to), and inward rectifier K(+) current (I K1). Qiliqiangxin can decrease I Na by 28.53% ± 5.98%, and its IC50 was 9.2 mg/L. 10 and 50 mg/L Qiliqiangxin decreased by 37.2% ± 6.4% and 55.9% ± 5.5% summit current density of I to. 10 and 50 mg/L Qiliqiangxin decreased I Ks by 15.51% ± 4.03% and 21.6% ± 5.6%. Qiliqiangxin represented a multifaceted pharmacological profile. The effects of Qiliqiangxin on Na and K currents of ventricular myocytes were more profitable in antiarrhythmic therapy in the clinic. We concluded that the relative efficacy of Qiliqiangxin was another choice for the existing antiarrhythmic therapy.
ABSTRACT
Qiliqiangxin capsule is newly developed Chinese patent drug and proved to be effective and safe for the treatment of patients with chronic heart failure. We compared the effects of different dose Qiliqiangxin on L type Ca(2+) current (I(Ca-L)) between normal and hypertrophied myocytes. A total of 40 healthy Sprague-Dawley rats were used in the study. The rats were randomly divided into two groups (control group and hypertrophy group). Cardiac hypertrophy was induced by pressure overload produced by partial ligation of the abdominal aorta. The control group was the sham-operated group. After 1 month, cardiac ventricular myocytes were isolated from the hearts of rats. Ventricular myocytes were exposed to 10 and 50 µmol/L Qiliqiangxin, and whole cell patch-clamp technique was used to study the effects of Qiliqiangxin on I(Ca-L). The current densities of I(Ca-L) were similar in control group (-12.70 ± 0.53 pA/pF, n = 12) and in hypertrophy group (-12.39 ± 0.62 pA/pF, n = 10). They were not statistically significant. 10 and 50 µmol/L Qiliqiangxin can decrease I(Ca-L) peak current 48.6%±16.8% and 59.0%±4.4% in control group. However, the peak current was only reduced 16.73%±8.03% by 50 µmol/L Qiliqiangxin in hypertrophied myocytes. The inhibited action of Qiliqiangxin on I(Ca-L) of hypertrophy group was lower than in control group. Qiliqiangxin affected L-type Ca(2+) channel and blocked I(Ca-L), as well as affected cardiac function finally. Qiliqiangxin has diphasic action that is either class IV antiarrhythmic agent or the agent of effect cardiac function.
