ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Mitochondrial BKCa channels contribute to protection of cardiomyocytes isolated from chronically hypoxic rats.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 42 citations in OpenAlex.
- Chronic hypoxia protects the mouse heart from oxidative stress via HIF-1α-mitochondria crosstalk.Cellular and molecular life sciences : CMLS · 2026Article
- Cardioprotective Effect of Chronic Hypoxia Involves Inhibition of Mitochondrial Permeability Transition Pore Opening.Physiological research · 2024Article
- Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences.Physiological research · 2024Review
- External Hemin as an Inhibitor of Mitochondrial Large-Conductance Calcium-Activated Potassium Channel Activity.International journal of molecular sciences · 2022Article
- The effect of an adaptation to hypoxia on cardiac tolerance to ischemia/reperfusion.Journal of biomedical research · 2022Article
- Review
- Single channel properties of mitochondrial large conductance potassium channel formed by BK-VEDEC splice variant.Scientific reports · 2021Article
- BK in Double-Membrane Organelles: A Biophysical, Pharmacological, and Functional Survey.Frontiers in physiology · 2021Review
- Hypoxic Regulation of the Large-Conductance, Calcium and Voltage-Activated Potassium Channel, BK.Frontiers in physiology · 2021Review
- Flavonoids and Mitochondria: Activation of Cytoprotective Pathways?Molecules (Basel, Switzerland) · 2020Review
- Endogenous and Agonist-induced Opening of Mitochondrial Big Versus Small Ca2+-sensitive K+ Channels on Cardiac Cell and Mitochondrial Protection.Journal of cardiovascular pharmacology · 2017Article
- Upregulated ATF6 contributes to chronic intermittent hypoxia-afforded protection against myocardial ischemia/reperfusion injury.International journal of molecular medicine · 2016Article
- Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels.Biomolecules · 2015Review
- A hypoxic episode during cardiogenesis downregulates the adenosinergic system and alters the myocardial anoxic tolerance.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Bax inhibitor-1-mediated inhibition of mitochondrial Ca2+ intake regulates mitochondrial permeability transition pore opening and cell death.Scientific reports · 2014Article
- BK Channels in Cardiovascular Diseases and Aging.Aging and disease · 2013Article
- Physiology of potassium channels in the inner membrane of mitochondria.Pflugers Archiv : European journal of physiology · 2012Review
- Rottlerin increases cardiac contractile performance and coronary perfusion through BKCa++ channel activation after cold cardioplegic arrest in isolated hearts.Circulation · 2011Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Chronic hypoxia protects the heart against injury caused by acute oxygen deprivation, but its salutary mechanism is poorly understood. The aim was to find out whether cardiomyocytes isolated from chronically hypoxic hearts retain the improved resistance to injury and whether the mitochondrial large-conductance Ca2+-activated K+ (BKCa) channels contribute to the protective effect. Adult male rats were adapted to continuous normobaric hypoxia (inspired O2 fraction 0.10) for 3 wk or kept at room air (normoxic controls). Myocytes, isolated separately from the left ventricle (LVM), septum (SEPM), and right ventricle, were exposed to 25-min metabolic inhibition with sodium cyanide, followed by 30-min reenergization (MI/R). Some LVM were treated with either 30 μM NS-1619 (BKCa opener), or 2 μM paxilline (BKCa blocker), starting 25 min before metabolic inhibition. Cell injury was detected by Trypan blue exclusion and lactate dehydrogenase (LDH) release. Chronic hypoxia doubled the number of rod-shaped LVM and SEPM surviving the MI/R insult and reduced LDH release. While NS-1619 protected cells from normoxic rats, it had no additive salutary effect in the hypoxic group. Paxilline attenuated the improved resistance of cells from hypoxic animals without affecting normoxic controls; it also abolished the protective effect of NS-1619 on LDH release in the normoxic group. While chronic hypoxia did not affect protein abundance of the BKCa channel regulatory β1-subunit, it markedly decreased its glycosylation level. It is concluded that ventricular myocytes isolated from chronically hypoxic rats retain the improved resistance against injury caused by MI/R. Activation of the mitochondrial BKCa channel likely contributes to this protective effect.
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