Heart of the matter: Coronary dysfunction in metabolic syndrome

被引:54
作者
Berwick, Zachary C. [1 ]
Dick, Gregory M. [2 ]
Tune, Johnathan D. [1 ]
机构
[1] Indiana Univ Sch Med, Dept Cellular & Integrat Physiol, Indianapolis, IN 46202 USA
[2] W Virginia Univ, Sch Med, Ctr Cardiovasc & Resp Sci, Dept Exercise Physiol, Morgantown, WV 26506 USA
关键词
Coronary circulation; Neurohumoral factors; Obesity; Renin-angiotensin-aldosterone axis; Sympathetic activation; VASCULAR SMOOTH-MUSCLE; DEPENDENT K+-CHANNELS; LEFT-VENTRICULAR DYSFUNCTION; BLOOD-FLOW; ANGIOTENSIN-II; NITRIC-OXIDE; INSULIN-RESISTANCE; ENDOTHELIAL DYSFUNCTION; REACTIVE HYPEREMIA; CARDIOVASCULAR-DISEASE;
D O I
10.1016/j.yjmcc.2011.06.025
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Metabolic syndrome (MetS) is a collection of risk factors including obesity, dyslipidemia, insulin resistance/impaired glucose tolerance, and/or hypertension. The incidence of obesity has reached pandemic levels, as similar to 20-30% of adults in most developed countries can be classified as having MetS. This increased prevalence of MetS is critical as it is associated with a two-fold elevated risk for cardiovascular disease. Although the pathophysiology underlying this increase in disease has not been clearly defined, recent evidence indicates that alterations in the control of coronary blood flow could play an important role. The purpose of this review is to highlight current understanding of the effects of MetS on regulation of coronary blood flow and to outline the potential mechanisms involved. In particular, the role of neurohumoral modulation via sympathetic alpha-adrenoceptors and the renin-angiotensin-aldosterone system (RAAS) are explored. Alterations in the contribution of end-effector K+, Ca2+, and transient receptor potential (TRP) channels are also addressed. Finally, future perspectives and potential therapeutic targeting of the microcirculation in MetS are discussed. This article is part of a Special Issue entitled "Coronary Blood Flow". (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:848 / 856
页数:9
相关论文
共 171 条
[1]   Obesity cardiomyopathy: Pathophysiology and evolution of the clinical syndrome [J].
Alpert, MA .
AMERICAN JOURNAL OF THE MEDICAL SCIENCES, 2001, 321 (04) :225-236
[2]   EFFECT OF INHIBITION OF NITRIC-OXIDE FORMATION ON CORONARY BLOOD-FLOW DURING EXERCISE IN THE DOG [J].
ALTMAN, JD ;
KINN, J ;
DUNCKER, DJ ;
BACHE, RJ .
CARDIOVASCULAR RESEARCH, 1994, 28 (01) :119-124
[3]   Hypertension and obesity [J].
Aneja, A ;
El-Atat, F ;
McFarlane, S ;
Sowers, JR .
RECENT PROGRESS IN HORMONE RESEARCH, VOL 59: CARDIOVASCULAR ENDOCRINOLOGY & OBESITY, 2004, 59 :169-205
[4]   Mechanisms of coronary microvascular adaptation to obesity [J].
Bagi, Zsolt .
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2009, 297 (03) :R556-R567
[5]  
Bassenge E, 1990, Rev Physiol Biochem Pharmacol, V116, P77
[6]   Endothelial glycocalyx and coronary vascular permeability: the fringe benefit [J].
Becker, Bernhard F. ;
Chappell, Daniel ;
Jacob, Matthias .
BASIC RESEARCH IN CARDIOLOGY, 2010, 105 (06) :687-701
[7]  
Belin De Chantemele EJ, J MOL CELL IN PRESS
[8]   Obesity induced-insulin resistance causes endothelial dysfunction without reducing the vascular response to hindlimb ischemia [J].
Belin de Chantemele, Eric J. ;
Ali, M. Irfan ;
Mintz, James ;
Stepp, David W. .
BASIC RESEARCH IN CARDIOLOGY, 2009, 104 (06) :707-717
[9]   Altered Mechanism of Adenosine-Induced Coronary Arteriolar Dilation in Early-Stage Metabolic Syndrome [J].
Bender, Shawn B. ;
Tune, Johnathan D. ;
Borbouse, Lena ;
Long, Xin ;
Sturek, Michael ;
Laughlin, M. Harold .
EXPERIMENTAL BIOLOGY AND MEDICINE, 2009, 234 (06) :683-692
[10]   The vascular response to the K+ channel inhibitor 4-aminopyridine in hypertensive rats [J].
Berg, T .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2003, 466 (03) :301-310