首页> 外文期刊>Journal of the American Society of Hypertension : >Role of angiotensin II type 2 receptor during electrophysiological remodeling of left ventricular hypertrophic myocardium in spontaneously hypertensive rats
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Role of angiotensin II type 2 receptor during electrophysiological remodeling of left ventricular hypertrophic myocardium in spontaneously hypertensive rats

机译:血管紧张素II型受体在自发性高血压大鼠左心室肥厚性心肌电生理重塑过程中的作用

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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, I Na , I CaL , I to , 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 ? P ? to 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 ? to 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 ? CaL 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 ? CaL 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 ? Highlights ? The activation of angiotensin II type 2 receptor (AT2R) improved the density of I to . ? The stimulation AT2R decreased the density of I CaL . ? The stimulation of AT2R reduced the left ventricular mass index. ? The stimulation of AT2R decreased the membrane capacitance of cardiomyocyte. ? The stimulation of AT2R improved the ventricular fibrillation threshold.
机译:摘要目的是探讨血管紧张素II型受体在自发性高血压大鼠(SHR)中左心室肥厚心肌的电生理重塑过程中的作用。总共36岁,10周龄,雄性shrs分为三组:控制,缬沙坦和缬沙坦?+?pd123319组(每次n?= 12)。在8周后,还测量了收缩压,左心室质量指数,心室有效的耐火剂期和心室原纤化阈值(VFT)。同时,通过全细胞贴片夹具在左心室肌细胞中测量I Na,I Cal,I至和膜电容。 Valsartan的VFT高于对照(Valsartan Vs.控制:17.4? 。控制:14.7?±0.42 PA / PF与11.2?±0.15 PA / PF,P?缬沙坦的p?+ valsartan + +?PD123319(缬沙坦与缬沙坦?+?PD123319:14.7?± ?0.42 pa / pf与13.6?±0.30 pa / pf,p?valsartan的p?cal的控制(Valsartan与控制:?4.6?±0.2 pa / pf与α.6.9?±0.1 PA / PF,P?缬沙坦的Cal的缬沙坦?+?PD123319(Valsartan Vs. Valsartan?+?PD123319:?4.6?±0.2Pa / PF与... 5.4?±0.1 PA / PF, p?亮点?血管紧张素II型受体(AT2R)的激活改善了I的密度。ΔT2R的刺激降低了I Cal的密度。ΔT2R的刺激减少了左心室质量指数。ΔT2R刺激减少了心肌细胞的膜电容。ΔT2R的刺激改善了心室颤动临界点。

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