Downregulation of alpha7 nicotinic acetylcholine receptor in two-kidney one-clip hypertensive rats

BMC Cardiovascular Disorders

Research Article

Ting Zhao¹  Fu-Ming Shen¹  Dong-Jie Li¹  Ji-Kuai Chen¹  Xia Tao²  Min Ni² 

[1] Department of Pharmacology, School of Pharmacy, Second Military Medical University, 200433, Shanghai, China;Department of Pharmacy, Changzheng Hospital, Second Military Medical University, 200003, Shanghai, China;

关键词: α7nAChR;    2K1C;    Vagus nerve function;    Tumor necrosis factor-α;   

DOI  :  10.1186/1471-2261-12-38

 received in 2012-03-21, accepted in 2012-05-18,  发布年份 2012

来源: Springer

【 摘 要 】

BackgroundInflammation processes are important participants in the pathophysiology of hypertension and cardiovascular diseases. The role of the alpha7 nicotinic acetylcholine receptor (α7nAChR) in inflammation has recently been identified. Our previous study has demonstrated that the α7nAChR-mediated cholinergic anti-inflammatory pathway is impaired systemically in the genetic model of hypertension. In this work, we investigated the changes of α7nAChR expression in a model of secondary hypertension.MethodsThe 2-kidney 1-clip (2K1C) hypertensive rat model was used. Blood pressure, vagus nerve function, serum tumor necrosis factor-α (TNF-α) and both the mRNA and protein levels of α7nAChR in tissues from heart, kidney and aorta were measured at 4, 8 and 20 weeks after surgery.ResultsCompared with age-matched control, it was found that vagus nerve function was significantly decreased in 2K1C rats with the development of hypertension. Serum levels of TNF-α were greater in 2K1C rats than in age-matched control at 4, 8 and 20 weeks. α7nAChR mRNA in the heart was not altered in 2K1C rats. In the kidney of 2K1C rats, α7nAChR expression was significantly decreased at 8 and 20 weeks, but markedly increased at 4 weeks. α7nAChR mRNA was less in aorta of 2K1C rats than in age-matched control at 4, 8 and 20 weeks. These findings were confirmed at the protein levels of α7nAChR.ConclusionsOur results suggested that secondary hypertension may induce α7nAChR downregulation, and the decreased expression of α7nAChR may contribute to inflammation in 2K1C hypertension.

【 授权许可】

Unknown   
© Chen et al.; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.