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Mitochondrial BKCa channels contribute to protection of cardiomyocytes isolated from chronically hypoxic rats

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, SAI}
Source Title	American Journal of Physiology-Heart and Circulatory Physiology. - : American Physiological Society - ISSN 0363-6135 Roč. 300, č. 2 (2011), H507-H513
Number 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

Number of the records: 1