Endothelium-Derived Hyperpolarization and Coronary Vasodilation: Diverse and Integrated Roles of Epoxyeicosatrienoic Acids, Hydrogen Peroxide, and Gap Junctions

Autor:	Yanping Liu, Jamie Y. Jeremy, Shaun L. Sandow, Nilima Shukla, David C. Ellinsworth, David D. Gutterman
Rok vydání:	2016
Předmět:	0301 basic medicine medicine.medical_specialty Endothelium-derived hyperpolarizing factor Endothelium Physiology Vasodilation 030204 cardiovascular system & hematology Biology Muscle Smooth Vascular Article Nitric oxide 03 medical and health sciences Transient receptor potential channel chemistry.chemical_compound 0302 clinical medicine Physiology (medical) Internal medicine medicine Animals Humans Calcium Signaling Molecular Biology Calcium signaling Myocardium Gap Junctions Hydrogen Peroxide Hyperpolarization (biology) Coronary Vessels Cell biology 030104 developmental biology Endocrinology medicine.anatomical_structure chemistry cardiovascular system Eicosanoids Endothelium Vascular Cardiology and Cardiovascular Medicine Intracellular
Zdroj:	Microcirculation. 23:15-32
ISSN:	1073-9688
DOI:	10.1111/micc.12255
Popis:	Myocardial perfusion and coronary vascular resistance are regulated by signalling metabolites released from the local myocardium that act either directly on the vascular smooth muscle cells (VSMC) or indirectly via stimulation of the endothelium. A prominent mechanism of vasodilation is endothelium-derived hyperpolarization (EDH) of the arteriolar smooth muscle, with epoxyeicosatrienoic acids (EETs) and hydrogen peroxide (H2O2) playing important roles in EDH in the coronary microcirculation. In some cases, EETs and H2O2 are released as transferable hyperpolarizing factors (EDHFs) that act directly on the VSMCs. By contrast, EETs and H2O2 can also promote endothelial Ca2+-activated K+ channel activity secondary to the amplification of extracellular Ca2+ influx and Ca2+ mobilization from intracellular stores, respectively. The resulting endothelial hyperpolarization may subsequently conduct to the media via myoendothelial gap junctions, or potentially lead to the release of a chemically-distinct factor(s). Furthermore, in human isolated coronary arterioles dilator signalling involving EETs and H2O2 may be integrated; being either complimentary or inhibitory depending on the stimulus. With an emphasis on the human coronary microcirculation, this review addresses the diverse and integrated mechanisms by which EETs and H2O2 regulate vessel tone, and also examines the hypothesis that myoendothelial microdomain signalling facilitates EDH activity in the human heart.
Databáze:	OpenAIRE
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