变时性
心力衰竭
肾上腺素能受体
变向性
卢西特里普
内科学
受体
内分泌学
肾上腺素能的
下调和上调
儿茶酚胺
α-1A肾上腺素能受体
信号转导
脱敏(药物)
α-1B肾上腺素能受体
医学
化学
生物
细胞生物学
心率
β-3肾上腺素能受体
舒张期
血压
生物化学
基因
作者
Nazha Hamdani,Wolfgang A. Linke
出处
期刊:Current Pharmaceutical Biotechnology
[Bentham Science]
日期:2012-12-11
卷期号:13 (13): 2522-2531
被引量:11
标识
DOI:10.2174/1389201011208062522
摘要
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. Keywords: Heart failure, β adrenergic receptors, myofilament proteins, cardiomyocytes
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