ArticleThe Journal of physiology2004
Mitochondrial modulation of Ca2+ sparks and transient KCa currents in smooth muscle cells of rat cerebral arteries.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 92 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Synaptic-like transmission between neural axons and arteriolar smooth muscle cells drives cerebral neurovascular coupling.Nature neuroscience · 2024Article
- Role of ryanodine receptor 2 and FK506-binding protein 12.6 dissociation in pulmonary hypertension.The Journal of general physiology · 2023Article
- Article
- Calcium and Reactive Oxygen Species Signaling Interplays in Cardiac Physiology and Pathologies.Antioxidants (Basel, Switzerland) · 2023Review
- Detrimental effects of transient cerebral ischemia on middle cerebral artery mitochondria in female rats.American journal of physiology. Heart and circulatory physiology · 2022Article
- MicroRNA-210-mediated mtROS confer hypoxia-induced suppression of STOCs in ovine uterine arteries.British journal of pharmacology · 2022Article
- Fetal Cerebral Artery Mitochondrion as Target of Prenatal Alcohol Exposure.International journal of environmental research and public health · 2019Review
- Mitochondrial ATP production provides long-range control of endothelial inositol trisphosphate-evoked calcium signaling.The Journal of biological chemistry · 2019Article
- The effects of mitochondrial inhibitors on CaCell calcium · 2018Article
- The large-conductance voltage- and CaThe Journal of physiology · 2018Article
- Mitochondrial calcium homeostasis: Implications for neurovascular and neurometabolic coupling.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Review
- Calcium Channels in Vascular Smooth Muscle.Advances in pharmacology (San Diego, Calif.) · 2017Review
- Role of Mitochondria in Cerebral Vascular Function: Energy Production, Cellular Protection, and Regulation of Vascular Tone.Comprehensive Physiology · 2016Review
- The mitochondrial function of the cerebral vasculature in insulin-resistant Zucker obese rats.American journal of physiology. Heart and circulatory physiology · 2016Article
- Mitochondrial ROS versus ER ROS: Which Comes First in Myocardial Calcium Dysregulation?Frontiers in cardiovascular medicine · 2016Article
- Dynamics of enhanced mitochondrial respiration in female compared with male rat cerebral arteries.American journal of physiology. Heart and circulatory physiology · 2015Article
- Mitochondria-derived ROS bursts disturb Ca²⁺ cycling and induce abnormal automaticity in guinea pig cardiomyocytes: a theoretical study.American journal of physiology. Heart and circulatory physiology · 2015Article
- Interaction between endoplasmic/sarcoplasmic reticulum stress (ER/SR stress), mitochondrial signaling and Ca(2+) regulation in airway smooth muscle (ASM).Canadian journal of physiology and pharmacology · 2015Review
- Diversity of mitochondria-dependent dilator mechanisms in vascular smooth muscle of cerebral arteries from normal and insulin-resistant rats.American journal of physiology. Heart and circulatory physiology · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria sequester and release calcium (Ca(2+)) and regulate intracellular Ca(2+) concentration ([Ca(2+)](i)) in eukaryotic cells. However, the regulation of different Ca(2+) signalling modalities by mitochondria in smooth muscle cells is poorly understood. Here, we investigated the regulation of Ca(2+) sparks, Ca(2+) waves and global [Ca(2+)](i) by mitochondria in cerebral artery smooth muscle cells. CCCP (a protonophore; 1 microm) and rotenone (an electron transport chain complex I inhibitor; 10 microm) depolarized mitochondria, reduced Ca(2+) spark and wave frequency, and elevated global [Ca(2+)](i) in smooth muscle cells of intact arteries. In voltage-clamped (-40 mV) cells, mitochondrial depolarization elevated global [Ca(2+)](i), reduced Ca(2+) spark amplitude, spatial spread and the effective coupling of sparks to large-conductance Ca(2+)-activated potassium (K(Ca)) channels, and decreased transient K(Ca) current frequency and amplitude. Inhibition of Ca(2+) sparks and transient K(Ca) currents by mitochondrial depolarization could not be explained by a decrease in intracellular ATP or a reduction in sarcoplasmic reticulum Ca(2+) load, and occurred in the presence of diltiazem, a voltage-dependent Ca(2+) channel blocker. Ru360 (10 microm), a mitochondrial Ca(2+) uptake blocker, and lonidamine (100 microm), a permeability transition pore (PTP) opener, inhibited transient K(Ca) currents similarly to mitochondrial depolarization. In contrast, CGP37157 (10 microm), a mitochondrial Na(+)-Ca(2+) exchange blocker, activated these events. The PTP blockers bongkrekic acid and cyclosporin A both reduced inhibition of transient K(Ca) currents by mitochondrial depolarization. These results indicate that mitochondrial depolarization leads to a voltage-independent elevation in global [Ca(2+)](i) and Ca(2+) spark and transient K(Ca) current inhibition. Data also suggest that mitochondrial depolarization inhibits Ca(2+) sparks and transient K(Ca) currents via PTP opening and a decrease in intramitochondrial [Ca(2+)].
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