Department of Cardiovascular Physiology, Institute of Physiology, Ruhr University Bochum, MA 3/56, D-44780 Bochum, Germany.
Curr Pharm Biotechnol. 2012 Oct;13(13):2522-31.
Heart failure is characterized by elevated circulating catecholamine levels and extensive abnormalities in β-adrenergic receptor signaling. Under physiological conditions, sympathetic modulation via catecholamines induces positive inotropic, chronotropic and lusitropic responses. Well established in heart failure patients is a pronounced activation of the sympathetic system, accompanied by downregulation and desensitization of β-adrenergic receptors, leading to a markedly diminished β-adrenergic contractile response. In this review, we will discuss the normal β-adrenergic receptor signaling pathway in the heart and focus on the pathphysiological alterations of β-adrenergic receptor signaling and contractile proteins in heart failure.
心力衰竭的特征是循环儿茶酚胺水平升高和β-肾上腺素能受体信号广泛异常。在生理条件下，儿茶酚胺通过交感神经调节诱导正性变力、变时和变松弛反应。在心力衰竭患者中，交感神经系统的显著激活已得到充分证实，同时β-肾上腺素能受体的下调和脱敏也随之发生，导致β-肾上腺素能收缩反应明显减弱。在这篇综述中，我们将讨论心脏中正常的β-肾上腺素能受体信号通路，并重点关注心力衰竭中β-肾上腺素能受体信号和收缩蛋白的病理生理改变。
