http://www.abbs.info      E-mail: [email protected]

ISSN 1672-9145                                                Acta Biochim Biophys Sin 2004, 36(12): 793–797                                                  CN 31-1940/Q


Changes in Autoantibodies against b1-Adrenoceptor and M2-Muscarinic Receptor during Development of Renovascular Hypertension in Rats

Jian-Ming ZHI*, Rong-Fang CHEN1, Heng WU2, Hui-Rong LIU2, and Rong-Rui ZHAO2

 

Department of Physiology, Shanghai Second Medical University, Shanghai 200025, China;

1Department of Toxicology, Second Military Medical University, Shanghai 200433, China;

2Department of Physiology, Shanxi Medical University, Taiyuan 030001, China

 

Abstract        In an experimental rat's renovascular hypertension model, we studied the genesis of anti-cardiac b1-adrenoceptor and M2-muscarinic receptor autoantibodies in relation to the changes in immunological function during the development of renal hypertension. The biological activities of these autoantibodies were also examined. It was shown that after two weeks of operation both the frequency of occurrence and the titre of autoantibodies to cardiac b1-adrenoceptor and M2-muscarinic receptor were significantly increased as compared with the control of pre-treatment. The increased autoantibodies lasted for several weeks and then automatically decreased gradually to the pre-clipping level at 10 weeks. Meanwhile the ratio of CD4+/CD8+ was also undergone an initial increase followed by gradual recovery and correlated well with the changes in antibody titre. The biological effects of these autoantibodies displayed an agonistic-like activities on the beating frequency of cultured neonatal cardiomyocyte. It is suggested that autoimmune mechanisms are involved in the pathogenesis of renal hypertension and the cardiac receptor autoantibodies might be one of the mechanisms leading to cardiac dysfunction.

 

Key words        autoantibody; renal hypertension; cardiac receptor; immunology

 

 

-----------------

Received: June 9, 2004        Accepted: October 2, 2004

*Corresponding author: Tel, 86-21-63846590-776446; E-mail, [email protected]