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. 2013 Jul 26;8(7):e70158. doi: 10.1371/journal.pone.0070158

Figure 5. Valsartan modulation of electrophysiological properties in vitro and in vivo.

Figure 5

A: Bar graph demonstrating average peak systolic amplitude of the calcium transients, expressed as absolute numbers from ratio between the peak of fluorescence intensity (F) and the intensity at rest (F0): AngII stimulation (10-6mol/L; 24 hours) augmented transients in cultured myocytes, which were attenuated by the AngII type 1 receptor blocker valsartan. Valsartan alone did not change the amplitude of calcium transient. The mean peak F/F0 was significantly higher in AngII–treated cells than control cells (*p<0.05 vs. all, # p<0.003 vs. Con and AngII). B: Ventricular effective refractory period (VERP) was dramatically reduced in LVH (37.3±3.4ms) compared to SHAM (52.3±2.6ms), SHAM+VAL (55.1±3.3ms), and LVH+VAL (51.9±2.9ms, *p<0.001 vs. all). C: Monophasic action potential duration at 90% repolarization (MAPD90) was significantly shortened in hypertrophic hearts (LVH= 44.0±4.3ms) as opposed to control groups (SHAM= 56.7±2.9ms; SHAM+VAL= 59.1±2.5ms), whereas valsartan significantly prolonged it (LVH+VAL= 55.6±4.3ms *p<0.001 vs. all). D through G: Representative endocardial ventriculograms recorded from the right ventricles indicating normal myocardial conduction in SHAM (panel D) and in SHAM+VAL (panel E), whereas conduction dispersion was observed in LVH (panel F) and LVH-VAL (panel G), the latter showing same duration in ventricular activation compared to SHAM and SHAM+VAL. Arrows indicate onset of ventricular depolarization, arrow-heads indicate end of ventricular depolarization, followed by abnormal repolarization in hypertrophic hearts, which was more pronounced in LVH (panel F, see Table 2 for data).