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Mitochondrial BKCa channels contribute to protection of cardiomyocytes isolated from chronically hypoxic rats
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SYSNO ASEP 0358912 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Mitochondrial BKCa channels contribute to protection of cardiomyocytes isolated from chronically hypoxic rats Author(s) Borchert, Gudrun H. (FGU-C)
Yang, Ch. (US)
Kolář, František (FGU-C) RID, ORCID, SAISource Title American Journal of Physiology-Heart and Circulatory Physiology. - : American Physiological Society - ISSN 0363-6135
Roč. 300, č. 2 (2011), H507-H513Number of pages 7 s. Language eng - English Country US - United States Keywords chronic hypoxia ; ventricular myocytes ; metabolic inhibition ; cell viability ; potassium channels Subject RIV FA - Cardiovascular Diseases incl. Cardiotharic Surgery R&D Projects GA305/07/1008 GA ČR - Czech Science Foundation (CSF) IAA500110804 GA AV ČR - Academy of Sciences of the Czech Republic (AV ČR) UT WOS 000287913700011 DOI 10.1152/ajpheart.00594.2010 Annotation Chronic hypoxia reduced glycosylation level of the beta-1 regulatory subunit of the cardiac mitochondrial large-conductance calcium-activated potassium channels (BK). Ventricular myocytes isolated from chronically hypoxic rats retained the improved resistance against injury caused by simulated ischemia/reperfusion. The blunting effect of paxilline (BK inhibitor) and the absence of additive protection by NS-1619 (BK opener) suggest that chronic hypoxia leads to the activation of these channels, which contribute to the protective mechanism Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2011
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