Journal of Capital Medical University ›› 2013, Vol. 34 ›› Issue (1): 140-143.doi: 10.3969/j.issn.1006-7795.2013.01.027

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Expression of α1A, β1 and β2 adrenergic receptors in rats lung with heart failure induced by myocardial infarction

JIANG Zhili1, LI Yanfang1, CAO Fangfang2, LIU Fei1, BAI Xueyuan3, LÜ Yang3   

  1. 1. Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China;
    2. Cardiac Surgery, Cardiovascular Institute and Fuwai Hospital, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing 100037, China;
    3. Department of Nephrology, The General Hospital of The People Liberation Army, Beijing 100853, China
  • Received:2012-05-08 Online:2013-02-21 Published:2013-02-25
  • Supported by:

    This study was supported by Chinese Integrated TCM-WM Scientific Research Foundation (2011-01).

Abstract:

Objective To investigate the protein levels of α1A1 and β2 adrenergic receptor ( AR ) in lungs of rats with chronic heart failure (CHF) induced by myocardial infarction. Methods Models of CHF established by anterior descending coronary artery ligature. Thirty five Wistar rats were randomly divided into three groups: control group (group A), sham operation group (group B) and CHF model group (group C). The protein expression levels of α1A-AR, β1-AR and β2-AR in lung tissue were measured by Western blotting.Results Compared with sham operation group,α1A-AR, β1-AR protein expression in group C markedly decreased (P<0.01 and P<0.05), expression of β2-AR remarkably increased (P<0.05), while there was no significant difference between control group and sham operation group (P>0.05). Conclusion CHF rats always had pulmonary congestion, the α1A-AR down-regulation helped pulmonary vascular relax and inhibited smooth muscle cells proliferation, which was a compensation of the pathological situation of CHF lung. Increasing expression of β2-AR in CHF lungs could relax the vascular and bronchial smooth muscle; promote the clearance of pulmonary edema fluid and lung conditions through opening the sodium ion channels and other mechanisms. It could also improve the permeability of the capillaries in lungs. The expression of β1-AR in CHF rats was down-regulated for negative feedback regulation of activation of the sympathetic adrenergic system or compensation of up-regulation of β2-AR,which could maintain a relatively stable rates of alveolar fluid clearance.

Key words: adrenergic receptor, lung, heart failure

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