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Sustained β1-Adrenergic Stimulation Modulates Cardiac Contractility by Ca2+/Calmodulin Kinase Signaling Pathway by Wang Wang, Weizhong Zhu, Shiqiang Wang, Dongmei Yang, Michael T. Crow, Rui-Ping Xiao, and Heping Cheng Circulation Research Volume 95(8):798-806 October 15, 2004 Copyright ? American Heart Association, Inc. All rights reserved. Figure 1. Sustained β1AR stimulation increased contraction amplitude and hastened relaxation in adult rat cardiomyocytes. Wang Wang et al. Circ Res. 2004;95:798-806 Copyright ? American Heart Association, Inc. All rights reserved. Figure 2. Effects of PKA and CaMKII inhibition on short-term and sustained β1AR contractile responses. Wang Wang et al. Circ Res. 2004;95:798-806 Copyright ? American Heart Association, Inc. All rights reserved. Figure 3. CaMKII-dependent increase of Ca2+ transients in response to sustained β1AR stimulation. Wang Wang et al. Circ Res. 2004;95:798-806 Copyright ? American Heart Association, Inc. All rights reserved. Figure 4. Effects of DN-CaMKII expression on short-term and sustained β1AR responses. Wang Wang et al. Circ Res. 2004;95:798-806 Copyright ? American Heart Association, Inc. All rights reserved. Figure 5. cAMP formation, CaMKII activity, and site-specific PLB phosphorylation during prolonged β1AR stimulation. Wang Wang et al. Circ Res. 2004;95:798-806 Copyright ? American Heart Association, Inc. All rights reserved. Figure 6. Role of cAMP/PKA in β1AR activation of CaMKII signaling. Wang Wang et al. Circ Res. 2004;95:798-806 Copyright ? American Heart Association, Inc. All rights reserved. Figure 1. Sustained β1AR stimulation increased contraction amplitude and hastened relaxation in adult rat cardiomyocytes. A and B, Typical chart recordings of cell shortening (0.5 Hz pacing) under short-term (10 minutes, A) and sustained (24 hour, B) exposure of cells to norepinephrine (NE, 100 nmol/L plus prazosin 1 μmol/L). Experimental protocols are shown on the top of the recordings. Downward defle
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