G
Guillermo J. Pérez
Researcher at University of Girona
Publications - 40
Citations - 2806
Guillermo J. Pérez is an academic researcher from University of Girona. The author has contributed to research in topics: BK channel & Brugada syndrome. The author has an hindex of 18, co-authored 36 publications receiving 2612 citations. Previous affiliations of Guillermo J. Pérez include Heidelberg University & University of Vermont.
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Journal ArticleDOI
Vasoregulation by the β1 subunit of the calcium-activated potassium channel
Robert Brenner,Guillermo J. Pérez,Adrian D. Bonev,Delrae M. Eckman,Jon C. Kosek,Steven W. Wiler,Andrew J. Patterson,Mark T. Nelson,Richard W. Aldrich +8 more
TL;DR: It is shown that targeted deletion of the gene for the β1 subunit leads to a decrease in the calcium sensitivity of BK channels, a reduction in functional coupling of calcium sparks to BK channel activation, and increases in arterial tone and blood pressure.
Journal ArticleDOI
Ionic and Cellular Basis for the Predominance of the Brugada Syndrome Phenotype in Males
José M. Di Diego,Jonathan M. Cordeiro,Robert J. Goodrow,Jeffrey M. Fish,Andrew C. Zygmunt,Guillermo J. Pérez,Fabiana S. Scornik,Charles Antzelevitch +7 more
TL;DR: The results suggest that the predominance of the Brugada phenotype in males is a result of the presence of a more prominent Ito in males versus females.
Journal ArticleDOI
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.
Journal ArticleDOI
Functional coupling of ryanodine receptors to KCa channels in smooth muscle cells from rat cerebral arteries.
TL;DR: The results indicate that the majority of ryanodine receptors that cause Ca2+ sparks are functionally coupled to KCa channels in the surface membrane, providing direct support for the idea that Ca2- sparks cause STOCs.
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Micromolar Ca2+ from sparks activates Ca2+-sensitive K+ channels in rat cerebral artery smooth muscle
TL;DR: The goal of the present study was to test the hypothesis that local Ca2+ release events (Ca2+ sparks) deliver high local Ca 2+concentration to activate nearby Ca1+-sensitive K+ channels in the BK channels.