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

Downregulation of alpha7 nicotinic acetylcholine receptor in two-kidney one-clip hypertensive rats.
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二肾一夹高血压大鼠α7烟碱乙酰胆碱受体的下调

DOI:
10.1186/1471-2261-12-38
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发表时间:
2012-06-08
影响因子:
2.1
通讯作者:
Shen FM
Shen FM
中科院分区:
医学4区
文献类型:
--
作者:
Chen JK;Zhao T;Ni M;Li DJ;Tao X;Shen FM

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炎症过程是高血压和心血管疾病的重要病理生理学过程。最近发现α7烟碱型乙酰胆碱受体(α7nAChR)在炎症中的作用。我们先前的研究已经证明,在高血压的遗传模型中,α7nAChR介导的胆碱能抗炎途径受到系统性损害。在本工作中,我们研究了α7nAChR在继发性高血压模型中的表达变化。采用二肾一夹(2K1C)高血压大鼠模型。分别于术后4、8、20周测定血压、迷走神经功能、血清肿瘤坏死因子-α(肿瘤坏死因子-α)及心脏、肾脏和主动脉组织中α7nAChR的基因和蛋白水平。与年龄匹配的对照组相比,2K1C大鼠的迷走神经功能随着高血压的发展而显著降低。2K1C组大鼠血清肿瘤坏死因子-α水平在第4、8、20周显著高于同龄对照组。2K1C大鼠心脏α7nAChR基因表达无明显变化。在2K1C大鼠的肾脏中,α7nAChR的表达在8周和20周时显著降低,而在4周时显著增加。2K1C组大鼠4周、8周和20周时,α-7nAChR m RNA在主动脉中的表达均低于年龄匹配的对照组。这些发现在α7nAChR蛋白水平得到了证实。结果提示,继发性高血压可导致α7nAChR表达下调,α7nAChR表达降低可能参与2K1C高血压的炎症反应。
Inflammation 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. The 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. Compared 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. Our results suggested that secondary hypertension may induce α7nAChR downregulation, and the decreased expression of α7nAChR may contribute to inflammation in 2K1C hypertension.
DOI: 10.1002/eji.201040540
发表时间: 2010-09
影响因子: 5.4
作者:
Pena, Geber;Cai, Bolin;Liu, Jun;van der Zanden, Esmerij P.;Deitch, Edwin A.;de Jonge, Wouter J.;Ulloa, Luis
通讯作者: Ulloa, Luis
DOI: 10.1291/hypres.27.193
发表时间: 2004-03-01
影响因子: 5.4
作者:
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通讯作者: Nishikawa, T
DOI: 10.1161/hypertensionaha.108.112706
发表时间: 2008-08-01
期刊: HYPERTENSION
影响因子: 8.3
作者:
Liao, Tang-Dong;Yang, Xiao-Ping;Carretero, Oscar A.
通讯作者: Carretero, Oscar A.
DOI: 10.1016/j.lfs.2007.01.026
发表时间: 2007-05-30
期刊: LIFE SCIENCES
影响因子: 6.1
作者:
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通讯作者: Kummer, Wolfgang
DOI: 10.1097/ccm.0b013e31819598f5
发表时间: 2009-02-01
影响因子: 8.8
作者:
Liu, Chong;Shen, Fu-Ming;Su, Ding-Feng
通讯作者: Su, Ding-Feng