ArticleCirculation research2005
Mitochondria-derived reactive oxygen species dilate cerebral arteries by activating Ca2+ sparks.
Article in Circulation research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 129 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Disrupted SR-Mitochondria Coupling Drives Ischemia-Reperfusion Vulnerability in the Middle-Aged Rat Heart.Biomedicines · 2026Article
- Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026Review
- Ethanol Exposure Increases Oxygen Consumption by Developing Cerebral Arteries in a Trimester-, Concentration- and Sex-Dependent Manner.Biomolecules · 2025Article
- Linoleic acid improves rosacea through repairing mitochondrial damage in keratinocytes.Life medicine · 2025Article
- Neurotoxic effects associated with chronic inhalation and oral exposure to glyphosate-based herbicide IN adult rats.Toxicology research · 2024Article
- Pulmonary hypertension associated with diazoxide: the SUR1 paradox.ERJ open research · 2023Review
- Oxidative Stress in a Mother Consuming Alcohol during Pregnancy and in Her Newborn: A Case Report.Antioxidants (Basel, Switzerland) · 2023Article
- Calcium and Reactive Oxygen Species Signaling Interplays in Cardiac Physiology and Pathologies.Antioxidants (Basel, Switzerland) · 2023Review
- Naringenin ameliorates homocysteine induced endothelial damage via the AMPKα/Sirt1 pathway.Journal of advanced research · 2021Article
- Lactate is an energy substrate for rodent cortical neurons and enhances their firing activity.eLife · 2021Article
- Aging-Induced Impairment of Vascular Function: Mitochondrial Redox Contributions and Physiological/Clinical Implications.Antioxidants & redox signaling · 2021Review
- Metabolic Reprogramming: Strategy for Ischemic Stroke Treatment by Ischemic Preconditioning.Biology · 2021Review
- Intermittent Hypoxia Augments Pulmonary Vasoconstrictor Reactivity through PKCβ/Mitochondrial Oxidant Signaling.American journal of respiratory cell and molecular biology · 2020Article
- Cerebrovascular function and mitochondrial bioenergetics after ischemia-reperfusion in male rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Fetal Cerebral Artery Mitochondrion as Target of Prenatal Alcohol Exposure.International journal of environmental research and public health · 2019Review
- SR-mitochondria communication in adult cardiomyocytes: A close relationship where the CaArchives of biochemistry and biophysics · 2019Review
- Molecular Bases of Brain Preconditioning.Frontiers in neuroscience · 2017Article
- Calcium Channels in Vascular Smooth Muscle.Advances in pharmacology (San Diego, Calif.) · 2017Review
- Mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone induces vasorelaxation without involving KBritish journal of pharmacology · 2016Article
8 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria regulate intracellular calcium (Ca2+) signals in smooth muscle cells, but mechanisms mediating these effects, and the functional relevance, are poorly understood. Similarly, antihypertensive ATP-sensitive potassium (KATP) channel openers (KCOs) activate plasma membrane KATP channels and depolarize mitochondria in several cell types, but the contribution of each of these mechanisms to vasodilation is unclear. Here, we show that cerebral artery smooth muscle cell mitochondria are most effectively depolarized by diazoxide (-15%, tetramethylrhodamine [TMRM]), less so by levcromakalim, and not depolarized by pinacidil. KCO-induced mitochondrial depolarization increased the generation of mitochondria-derived reactive oxygen species (ROS) that stimulated Ca2+ sparks and large-conductance Ca2+-activated potassium (KCa) channels, leading to transient KCa current activation. KCO-induced mitochondrial depolarization and transient KCa current activation were attenuated by 5-HD and glibenclamide, KATP channel blockers. MnTMPyP, an antioxidant, and Ca2+ spark and KCa channel blockers reduced diazoxide-induced vasodilations by >60%, but did not alter dilations induced by pinacidil, which did not elevate ROS. Data suggest diazoxide drives ROS generation by inducing a small mitochondrial depolarization, because nanomolar CCCP, a protonophore, similarly depolarized mitochondria, elevated ROS, and activated transient KCa currents. In contrast, micromolar CCCP, or rotenone, an electron transport chain blocker, induced a large mitochondrial depolarization (-84%, TMRM), reduced ROS, and inhibited transient KCa currents. In summary, data demonstrate that mitochondria-derived ROS dilate cerebral arteries by activating Ca2+ sparks, that some antihypertensive KCOs dilate by stimulating this pathway, and that small and large mitochondrial depolarizations lead to differential regulation of ROS and Ca2+ sparks.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.