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β-肾上腺素受体兴奋是心肌收缩力增强和心输出量增加的重要原因。但持续的β受体兴奋能够促进心脏的病理性改变,如心肌细胞肥大和细胞凋亡,这是慢性心功能不全的成因之一。心脏同时存在β1受体、β2受体和β3受体,分别激活不同的信号转导通路。β2受体的持续激活能使心肌通过Gi-磷酯酰肌醇3激酶-蛋白激酶B途径,防止心肌细胞的凋亡,而长期的β1受体激活能通过蛋白激酶A非依赖性的钙调素激酶Ⅱ途径,导致心肌细胞肥大和凋亡。这种受体亚型特异性的信号转导途径证实了应用兼有β2受体激动作用的β1受体阻断剂有助于慢性心功能不全的治疗。
β-adrenergic receptor excitability is an important reason for increased myocardial contractility and increased cardiac output. However, continuous β receptor activation can promote the pathological changes of heart, such as cardiomyocyte hypertrophy and apoptosis, which is one of the causes of chronic heart failure. At the same time, β1 receptor, β2 receptor and β3 receptor exist in the heart, which activate different signal transduction pathways respectively. Sustained activation of the β2 receptor prevents myocardial via apoptosis through the Gi- phosphatidylinositol 3-kinase-protein kinase B pathway, whereas long-term activation of the β1 receptor is mediated by protein kinase A-independent calcium regulation Suprase kinase pathway leads to cardiomyocyte hypertrophy and apoptosis. This receptor subtype-specific signal transduction pathway confirms that the use of β1 receptor blockers with β2 receptor agonism contributes to the treatment of chronic heart failure.