Vascular control in humans: focus on the coronary microcirculation

被引：65

作者：

Liu, Yanping ^{[2
]}

Gutterman, David D. ^{[1
,3
]}

机构：

[1] Med Coll Wisconsin, Milwaukee, WI 53226 USA

[2] NIH, Natl Ctr Res Resources, Bethesda, MD 20892 USA

[3] Med Coll Wisconsin, Dept Med & Cardiovasc Ctr, Vet Adm Med Ctr, Milwaukee, WI 53226 USA

来源：

BASIC RESEARCH IN CARDIOLOGY | 2009年 / 104卷 / 03期

关键词：

coronary circulation; myogenic response; flow-mediated dilation; EDHF; reactive oxygen species; diabetes; K+ channels; SENSITIVE POTASSIUM CHANNELS; EPOXYGENASE-DERIVED EICOSANOIDS; CA2+-ACTIVATED K+ CHANNELS; MESENTERIC SMALL ARTERIES; FLOW-INDUCED DILATION; SMOOTH-MUSCLE-CELLS; ENDOTHELIUM-DEPENDENT HYPERPOLARIZATION; LEFT-VENTRICULAR HYPERTROPHY; INTERNAL MAMMARY ARTERY; CAMP-MEDIATED DILATION;

D O I：

10.1007/s00395-009-0775-y

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Myocardial perfusion is regulated by a variety of factors that influence arteriolar vasomotor tone. An understanding of the physiological and pathophysiological factors that modulate coronary blood flow provides the basis for the judicious use of medications for the treatment of patients with coronary artery disease. Vasomotor properties of the coronary circulation vary among species. This review highlights the results of recent studies that examine the mechanisms by which the human coronary microcirculation is regulated in normal and disease states, focusing on diabetes. Multiple pathways responsible for myogenic constriction and flow-mediated dilation in human coronary arterioles are addressed. The important role of endothelium-derived hyperpolarizing factors, their interactions in mediating dilation, as well as speculation regarding the clinical significance are emphasized. Unique properties of coronary arterioles in human vs. other species are discussed.

引用

页码：211 / 227

页数：17

共 156 条

[21] PRODUCTION OF SUPEROXIDE RADICALS AND HYDROGEN-PEROXIDE BY NADH-UBIQUINONE REDUCTASE AND UBIQUINOL-CYTOCHROME C REDUCTASE FROM BEEF-HEART MITOCHONDRIA [J].