G
George C. Wellman
Researcher at University of Vermont
Publications - 71
Citations - 4044
George C. Wellman is an academic researcher from University of Vermont. The author has contributed to research in topics: Cerebral arteries & Vasodilation. The author has an hindex of 32, co-authored 70 publications receiving 3727 citations. Previous affiliations of George C. Wellman include University of Leicester & Loma Linda University Medical Center.
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Journal ArticleDOI
Cerebral vasospasm following subarachnoid hemorrhage: time for a new world of thought.
Ryszard M. Pluta,Jacob Hansen-Schwartz,Jens P. Dreier,Peter Vajkoczy,R. Loch Macdonald,Shigeru Nishizawa,Hideotoshi Kasuya,George C. Wellman,Emanuela Keller,Alois Zauner,Nicholas Dorsch,Joseph Clark,Shigeki Ono,Talat Kiris,Peter LeRoux,John H. Zhang +15 more
TL;DR: A key issue is the recognition of events other than arterial narrowing such as early brain injury and cortical spreading depression and of their contribution to overall mortality and morbidity.
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Targeted Disruption of Kir2.1 and Kir2.2 Genes Reveals the Essential Role of the Inwardly Rectifying K+ Current in K+-Mediated Vasodilation
TL;DR: K2.1 gene expression in arterial smooth muscle is required for Kir currents and K(+)-induced dilations in cerebral arteries and the complete absence of the open reading frame in animals homozygous for the targeted allele was confirmed.
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Ca2+ channels, ryanodine receptors and Ca(2+)-activated K+ channels: a functional unit for regulating arterial tone.
Jonathan H. Jaggar,George C. Wellman,Thomas J. Heppner,Valerie A. Porter,Guillermo J. Pérez,Maik Gollasch,Thomas Kleppisch,Michael Rubart,Andra S. Stevenson,W. J. Lederer,Harm J. Knot,Adrian D. Bonev,Mark T. Nelson +12 more
TL;DR: Using functional evidence from cardiac myocytes, and histological evidence from smooth muscle, it is explored whether Ca2+ channels, RyR channels, and KCa channels function as a coupled unit, through Ca2- and voltage, to regulate arterial smooth muscle membrane potential and vascular tone.
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Gender Differences in Coronary Artery Diameter Involve Estrogen, Nitric Oxide, and Ca2+-Dependent K+ Channels
TL;DR: It is proposed that physiological levels of circulating 17 beta-estradiol elevate basal NO release from the endothelial cells, which increases the diameter of pressurized coronary arteries and part of the effect of this NO is through activation of KCa channels in the smooth muscle cells of the coronary arteries.
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Signaling between SR and plasmalemma in smooth muscle: sparks and the activation of Ca2+-sensitive ion channels.
George C. Wellman,Mark T. Nelson +1 more
TL;DR: Ca2+ sparks are local Ca2+ signaling events that in smooth muscle can act on plasma membrane ion channels to influence excitation-contraction coupling as well as gene expression.