ArticleAmerican journal of physiology. Cell physiology2010
Mitochondrial matrix K+ flux independent of large-conductance Ca2+-activated K+ channel opening.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- BK Channels Orchestrate Cardiac Homeostasis Through Mitochondrial Uncoupling Proteins.bioRxiv : the preprint server for biology · 2026Article
- Inflammatory response to the ischaemia-reperfusion insult in the liver after major tissue trauma.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022Review
- Mitochondrial ion channels in cardiac function.American journal of physiology. Cell physiology · 2021Review
- Ketone Ester D-β-Hydroxybutyrate-(R)-1,3 Butanediol Prevents Decline in Cardiac Function in Type 2 Diabetic Mice.Journal of the American Heart Association · 2021Article
- Review
- Inhibition of Potassium Channels Affects the Ability of Pig Spermatozoa to Elicit Capacitation and Trigger the Acrosome Exocytosis Induced by Progesterone.International journal of molecular sciences · 2021Article
- Neuronal AMPK coordinates mitochondrial energy sensing and hypoxia resistance in C. elegans.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Mitochondrial light switches: optogenetic approaches to control metabolism.The FEBS journal · 2020Review
- Optogenetic control of mitochondrial protonmotive force to impact cellular stress resistance.EMBO reports · 2020Article
- CaBrain, behavior, and immunity · 2018Article
- Expression and Activation of BKFrontiers in cardiovascular medicine · 2018Article
- Slow CaFrontiers in physiology · 2018Article
- 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
- The Slo(w) path to identifying the mitochondrial channels responsible for ischemic protection.The Biochemical journal · 2017Review
- Identity and function of a cardiac mitochondrial small conductance CaBiochimica et biophysica acta. Bioenergetics · 2017Article
- The effect of respiration buffer composition on mitochondrial metabolism and function.PloS one · 2017Article
- Early effects of the antineoplastic agent salinomycin on mitochondrial function.Cell death & disease · 2015Article
- BKCa channel activation increases cardiac contractile recovery following hypothermic ischemia/reperfusion.American journal of physiology. Heart and circulatory physiology · 2015Article
- Mitochondrial BKCa channel.Frontiers in physiology · 2015Review
- Article
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Authors and funding
5 authors.
Funding
Abstract
Large-conductance Ca(2+)-activated K(+) channels (BK(Ca)) in the inner mitochondrial membrane may play a role in protecting against cardiac ischemia-reperfusion injury. NS1619 (30 microM), an activator of BK(Ca) channels, was shown to increase respiration and to stimulate reactive oxygen species generation in isolated cardiac mitochondria energized with succinate. Here, we tested effects of NS1619 to alter matrix K(+), H(+), and swelling in mitochondria isolated from guinea pig hearts. We found that 30 microM NS1619 did not change matrix K(+), H(+), and swelling, but that 50 and 100 microM NS1619 caused a concentration-dependent increase in matrix K(+) influx (PBFI fluorescence) only when quinine was present to block K(+)/H(+) exchange (KHE); this was accompanied by increased mitochondrial matrix volume (light scattering). Matrix pH (BCECF fluorescence) was decreased slightly by 50 and 100 microM NS1619 but markedly more so when quinine was present. NS1619 (100 microM) caused a significant leak in lipid bilayers, and this was enhanced in the presence of quinine. The K(+) ionophore valinomycin (0.25 nM), which like NS1619 increased matrix volume and increased K(+) influx in the presence of quinine, caused matrix alkalinization followed by acidification when quinine was absent, and only alkalinization when quinine was present. If K(+) is exchanged instantly by H(+) through activated KHE, then matrix K(+) influx should stimulate H(+) influx through KHE and cause matrix acidification. Our results indicate that KHE is not activated immediately by NS1619-induced K(+) influx, that NS1619 induces matrix K(+) and H(+) influx through a nonspecific transport mechanism, and that enhancement with quinine is not due to the blocking of KHE, but to a nonspecific effect of quinine to enhance current leak by NS1619.
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