作者: Adriana Adameova , Paramjit S. Tappia , Naranjan S. Dhalla
DOI: 10.1007/978-1-4614-5203-4_16
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摘要: Activation of the sympathetic nervous system (SNS) releases norepinephrine, stimulates β-adrenoceptors, and plays a crucial role in development cardiac hypertrophy upon activation various cellular signaling pathways heart. At early stages, norepinephrine-induced serves as an adaptive mechanism for maintaining heart function whereas at late it is associated with contractile dysfunction, alterations electrical activity, programmed cell death. G s -protein coupled β 1- or 2-adrenoceptors produces increase contractility some deleterious effects that i 2- 3-adrenoceptors known to result beneficial actions While involves downstream adenylyl cyclase (AC), -proteins either depression AC augmentation guanylate activity. In this article, we discuss physiological aspects β-adrenergic their modification hypertrophied well participation transition failure. Furthermore, highlight components β-adrenoreceptor cascade may participate genesis thus serve pharmacological targets prevention treatment failing