我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

盐皮质激素受体介导的糖皮质激素对心血管影响的病理生理学机制

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2012年第6期
页码:
780-783
栏目:
综述
出版日期:
2012-12-25

文章信息/Info

Title:
Pathophysiological mechanisms of mineralocorticoid receptor-mediated glucocorticoid effect on cardiovascular system
作者:
周玉文1; 2; 曹雪滨2
(1.保定市第二医院心内科，河北 保定 071051；2.解放军第252医院心内科，河北 保定 071000)
Author(s):
ZHOU Yu-wen1; 2;  CAO Xue-bin12
(1.Department of Cardiology, Hospital, Baoding 071051, Hebei, China; 2.Department of Cardiology, PLA 252 Hospital, Baoding 071000, Hebei, China)
关键词:
糖皮质激素; 盐皮质激素受体; 心血管
Keywords:
glucocorticoid;  mineralocorticoid receptor;  heart and blood vessel
分类号:
R997.11
DOI:
-
文献标识码:
A
摘要:
糖皮质激素（GC）由肾上腺合成分泌，也可在心肌中合成。GC和盐皮质激素(MC)对盐皮质激素受体(MR)具有同等的亲和力。心血管中存在MR。GC可通过与MR结合作用于心血管系统。心脏中的GC远远高于血液循环。氧化应激可促进MR的激活，而激活的MR又可诱导氧化应激，并参与心肌纤维化、心脏重构，促进钙离子内流。血清GC水平的升高是慢性心衰患者死亡风险增长的独立预测因子，具有致动脉粥样硬化，促进高血压形成的作用。阻滞MR已经作为房颤上游治疗的主要原则被论及GC在一些局部组织中浓度的增高与心血管高危因素有关。
Abstract:
Glucocorticoid (GC) is synthesized by the adrenal gland or in cardiac muscles. GC and mineralocorticoids (MC) have the same affinity for the mineralocorticoid receptor (MR). GC can act on cardiovascular system through binding to MR. GC in the heart is much higher than in the blood. GC activation can be accelerated by oxidative stress, and activated MR can also induce oxidative stress and is involved in myocardial fibrosis, cardiac remodeling and acceleration of calcium ion flow. Elevated serum GC level is an independent prediction factor of increased mortality risk in patients with chronic heart failure. Blocking MR has been reported as one main principle of “upstream” treatment of atrial fibrillation (AF). Elevated GC concentration in some local tissues is a cardiovascular risk factor.

参考文献/References

[1]Chai W,Hofland J,Jansen PM,et al.Steroidogenesis vs. steroid uptake in the heart:do corticosteroids mediate effects via cardiac mineralocorticoid receptors?[J].J Hypertens,2010,28(5):1044-1053.
[2]Reini SA,Wood CE,Keller-Wood M.The ontogeny of genes related to ovine fetal cardiac growth[J].Gene Expr Patterns,2009,9(2):122-128.
[3]Ohtani T, Mano T,Hikoso S,et al.Cardiac steroidogenesis and glucocorticoid in the development of cardiac hypertrophy during the progression to heart failure[J].J Hypertens,2009,27(5):1074-1083.
[4]Taves MD,Gomez-Sanchez CE,Soma KK.Extra-adrenal glucocorticoids and mineralocorticoids:evidence for local synthesis,regulation, and function[J].Am J Physiol Endocrinol Metab,2011,301(1):E11-E24.
[5]Yamaji M,Tsutamoto T,Kawahara C,et al.Serum cortisol as a useful predictor of cardiac events in patients with chronic heart failure: the impact of oxidative stress[J].Circ Heart Fail,2009,2(6):608-615.
[6]Costantini D,Marasco V,Moller AP.A meta-analysis of glucocorticoids as modulators of oxidative stress in vertebrates[J].J Comp Physiol B, 2011,181(4):447-456.
[7]Zafir A,Banu N.Modulation of in vivo oxidative status by exogenous corticosterone and restraint stress in rats[J].Stress,2009,12(2):167-177.
[8]Balkaya M,Prinz V,Custodis F,et al.Stress worsens endothelial function and ischemic stroke via glucocorticoids[J].Stroke,2011,42(11):3258-3264.
[9]Wilson P,Morgan J,Funder JW,et al. Mediators of mineralocorticoid receptor-induced profibrotic inflammatory responses in the heart[J].Clin Sci(Lond),2009,116(9):731-739.
[10]Martin-Fernandez B,de las Heras N,Miana M, et al.Structural, functional, and molecular alterations produced by aldosterone plus salt in rat heart:association with enhanced serum and glucocorticoid-regulated kinase-1 expression[J].J Cardiovasc Pharmacol,2011,57(1):114-121.
[11]Wagner M,Rudakova E,Volk T.Aldosterone-induced changes in the cardiac L-type Ca(2+) current can be prevented by antioxidants in vitro and are absent in rats on low salt diet[J].Pflugers Arch,2008,457(2):339-349.
[12]Guder G,Bauersachs J,Frantz S,et al.Complementary and incremental mortality risk prediction by cortisol and aldosterone in chronic heart failure[J].Circulation,2007,115(13):1754-1761.
[13]Yamaji M,Tsutamoto T,Kawahara C,et al.Serum cortisol as a useful predictor of cardiac events in patients with chronic heart failure: the impact of oxidative stress[J].Circ Heart Fail,2009,2(6):608-615.
[14]Lother A,Berger S,Gilsbach R,et al.Ablation of mineralocorticoid receptors in myocytes but not in fibroblasts preserves cardiac function[J].Hypertension,2011,57(4):746-754.
[15]Fraccarollo D,Berger S,Galuppo P,et al.Deletion of cardiomyocyte mineralocorticoid receptor ameliorates adverse remodeling after myocardial infarction[J].Circulation,2011,123(4):400-408.
[16]Yamaji M,Tsutamoto T,Kawahara C,et al.Serum cortisol as a useful predictor of cardiac events in patients with chronicheart failure: the impact of oxidative stress[J].Circ Heart Fail,2009,2(6):608-615.
[17]Deuchar GA,McLean D,Hadoke PW,et al.11beta-hydroxysteroid dehydrogenase type 2 deficiency accelerates atherogenesis and causes proinflammatory changes in the endothelium in apoe-/- mice[J].Endocrinology,2011,152(1):236-246.
[18]Goodwin JE,Zhang J, Gonzalez D,et al.Knockout of the vascular endothelial glucocorticoid receptor abrogates dexamethasone-induced hypertension[J].J Hypertens,2011,29(7):1347-1356.

备注/Memo

备注/Memo:
收稿日期：2012-03-22.基金项目：军队中医药科研专项课题项目资助（10zyz106） 通讯作者：曹雪滨，教授，主要从事心力衰竭的研究 Email：cxb@yahoo.com.cn 作者简介：周玉文，硕士生 Email：438710374@qq.com
更新日期/Last Update: 2012-12-30