【摘要】 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。

    Cardiac βadrenoceptor subtypes and chronic heart failure  LIU Xin1, KANG Yi2. 1. Department of Pathophysiology; 2. Department of Pharmacology, Tianjin Medical University, Tianjin 300070, China

    Abstract：  βadrenoceptor stimulation serves as the most powerful means to increase both the cardiac contractile and cardiac output in response to stress or exercise. However, sustained βadrenoceptor stimulation promotes pathological cardiac remodeling such as myocyte hypertrophy and apoptosis, which contributes to heart failure. Coexisting cardiac βadrenoceptor subtypes, mainly β1,β2and β3 adrenoceptors, activate different signaling cascades. As a result, sustained β2adrenoceptor stimulation protects cardiomyocytes against apoptosis via a Giphosphatidylinositol 3kinaseprotein kinase B pathway,  whereas chronic β1adrenoceptor stimulation induces myocyte hypertrophy and apoptosis by protein kinase Aindependent activation of calmodulin kinase Ⅱ signaling. The mechanisms mentioned above help us to understand that β blockers with β2adrenoceptor activation is beneficial to chronic heart failure.

     

 

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