Valsartan improves the electrophysiological characteristics of left ventricular hypertrophic myocardium in spontaneously hypertensive rats.
The objective was to investigate the effects of valsartan on the electrophysiological characteristics of left ventricular hypertrophic myocardium in spontaneously hypertensive rats (SHR). A total of 24 10-week-old male SHR were divided into two groups: valsartan and non-valsartan groups (n=12 in each). Twelve 10-week-old Wistar-Kyoto rats were served as the control group. Kv4.2 expression was measured in left ventricular myocardium using western blots. In addition, the systolic blood pressure, left ventricular mass index (LVMI), ventricular effective refractory period and ventricular fibrillation threshold (VFT) were also measured after eight weeks. INa, ICaL, Ito and membrane capacitance were measured in left ventricular myocytes after 8 weeks by whole-cell patch clamp. Valsartan decreased LVMI compared with the non-Valsartan group (Valsartan vs. non-Valsartan: 3.2±0.03 mg g(-1) vs. 3.7±0.02 mg g(-1), P<0.01). Valsartan also enhanced the VFT compared with the non-Valsartan group (Valsartan vs. non-Valsartan: 18.6±0.3 mA vs. 15.4±0.4 mA, P<0.01). The expression of Kv4.2 was significantly lower in the non-Valsartan and Valsartan groups compared with the control group (P<0.01). The expression of Kv4.2 was significantly higher in the Valsartan group compared with the non-Valsartan group (P<0.01). Valsartan decreased the density of ICaL compared with non-Valsartan group (Valsartan vs. non-Valsartan: -5.5±0.6 pA/pF vs. -7.2±0.9 pA/pF, P<0.05). Valsartan improved the density of Ito compared with non-Valsartan group(Valsartan vs. non-Valsartan: 13.93±0.8 pA/pF vs. 11.22±1.0 pA/pF, P<0.05). Valsartan improves the electrophysiological characteristics of left ventricular hypertrophic myocardium in spontaneously hypertensive rat.
Department of Cardiology, The First Affiliated Hospital, Sun Yat-sen University of Medical Sciences, Guangzhou, China.
Huang
H
Zhi-Bin
Department of Cardiology, The Sun Yat-sen Memorial Hospital, Sun Yat-sen University of Medical Sciences, Guangzhou, China.
Fang
F
Chang
Department of Cardiology, The Sun Yat-sen Memorial Hospital, Sun Yat-sen University of Medical Sciences, Guangzhou, China.
Lin
L
Mao-Huan
Department of Cardiology, The Sun Yat-sen Memorial Hospital, Sun Yat-sen University of Medical Sciences, Guangzhou, China.
Yuan
Y
Gui-Yi
Department of Cardiology, The Sun Yat-sen Memorial Hospital, Sun Yat-sen University of Medical Sciences, Guangzhou, China.
Zhou
Z
Shu-Xian
Department of Cardiology, The Fifth Affiliated Hospital, Sun Yat-sen University of Medical Sciences, Zhuhai, China.
Wu
W
Wei
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D006352:Heart Ventricles / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR; D051672:Shal Potassium Channels / Q000378:metabolism; D013777:Tetrazoles / Q000494:pharmacology*; D014633:Valine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000068756:Valsartan
D051672:Shal Potassium Channels; D013777:Tetrazoles; D000068756:Valsartan; D014633:Valine