Abstract
The objective was to investigate the role of angiotensin II type 2 receptor during electrophysiological remodeling of left ventricular hypertrophic myocardium in spontaneously hypertensive rats (SHRs). A total of 36, aged 10 weeks, male SHRs were divided into three groups: control, valsartan, and valsartan + PD123319 groups (n = 12 in each). The systolic blood pressure, left ventricular mass index, ventricular effective refractory period, and ventricular fibrillation threshold (VFT) were also measured after 8 weeks. At the same time, INa, ICaL, Ito, and membrane capacitance were measured in left ventricular myocytes by whole-cell patch-clamp. The VFT of valsartan was higher than that of control (valsartan vs. control: 17.4 ± 0.6 mA vs. 15.8 ± 0.5 mA, P < .05). The VFT of valsartan was higher than that of valsartan + PD123319 (valsartan vs. valsartan + PD123319: 17.4 ± 0.6 mA vs. 16.6 ± 0.9 mA, P < .05). The density of Ito of valsartan was higher than that of control (valsartan vs. control: 14.7 ± 0.42 pA/pF vs. 11.2 ± 0.15 pA/pF, P < .05). The density of Ito of valsartan was higher than that of valsartan + PD123319 (valsartan vs. valsartan + PD123319: 14.7 ± 0.42 pA/pF vs. 13.6 ± 0.30 pA/pF, P < .05). The density of ICaL of valsartan was lower than that of control (valsartan vs. control: −4.6 ± 0.2 pA/pF vs. −6.9 ± 0.1 pA/pF, P < .05). The density of ICaL of valsartan was lower than that of valsartan + PD123319 (valsartan vs. valsartan + PD123319: −4.6 ± 0.2 pA/pF vs. −5.4 ± 0.1 pA/pF, P < .05). These results demonstrated that the stimulation of angiotensin II type 2 receptor improved electrophysiological remodeling of left ventricular hypertrophic myocardium in SHR.
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