ArticleThe Journal of physiology2001
Mitochondria regulate inactivation of L-type Ca2+ channels in rat heart.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Calcium and arrhythmogenesis.Physiological reviews · 2007Pooled it
- The NADPH oxidase inhibitor diphenyleneiodonium suppresses CaThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- Mitochondrial clearance of calcium facilitated by MICU2 controls insulin secretion.Molecular metabolism · 2021Article
- Modulations of Cardiac Functions and Pathogenesis by Reactive Oxygen Species and Natural Antioxidants.Antioxidants (Basel, Switzerland) · 2021Review
- CaCells · 2019Review
- Pharmacological Preconditioning Using Diazoxide Regulates Store-Operated CaFrontiers in physiology · 2019Article
- Article
- Calcium transport across the inner mitochondrial membrane: molecular mechanisms and pharmacology.Molecular and cellular endocrinology · 2012Review
- Pharmacological preconditioning by diazoxide downregulates cardiac L-type Ca(2+) channels.British journal of pharmacology · 2010Article
- Calcium balance and mechanotransduction in rat cochlear hair cells.Journal of neurophysiology · 2010Article
- Mitochondrial ryanodine receptors and other mitochondrial Ca2+ permeable channels.FEBS letters · 2010Review
- Mitochondria in cardiomyocyte Ca2+ signaling.The international journal of biochemistry & cell biology · 2009Review
- In vitro intracellular trafficking of virulence antigen during infection by Yersinia pestis.PloS one · 2009Article
- Mitochondrial Ca2+ uptake: tortoise or hare?Journal of molecular and cellular cardiology · 2009Article
- 'Pressure-flow'-triggered intracellular Ca2+ transients in rat cardiac myocytes: possible mechanisms and role of mitochondria.The Journal of physiology · 2008Article
- Mechanisms of reduced mitochondrial Ca2+ accumulation in failing hamster heart.Pflugers Archiv : European journal of physiology · 2007Article
- Calmodulin kinase II accelerates L-type Ca2+ current recovery from inactivation and compensates for the direct inhibitory effect of [Ca2+]i in rat ventricular myocytes.The Journal of physiology · 2006Article
- Modulation of synaptic transmission by the BCL-2 family protein BCL-xL.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Mechano-oxidative coupling by mitochondria induces proinflammatory responses in lung venular capillaries.The Journal of clinical investigation · 2003Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
1. L-type Ca2+ channels play an important role in vital cell functions such as muscle contraction and hormone secretion. Both a voltage-dependent and a Ca2+-dependent process inactivate these channels. Here we present evidence that inhibition of the mitochondrial Ca2+ import mechanism in rat (Sprague-Dawley) ventricular myocytes by ruthenium red (RR), by Ru360 or by carbonyl cyanide m-chlorophenylhydrazone (CCCP) decreases the magnitude of electrically evoked transient elevations of cytosolic Ca2+ concentration ([Ca2+]c). These agents were most effective at stimulus rates greater than 1 Hz. 2. RR and CCCP also caused a significant delay in the recovery from inactivation of L-type Ca2+ currents (I(Ca)). This suggests that sequestration of cytosolic Ca2+, probably near the mouth of L-type Ca2+ channels, into mitochondria during cardiac contractile cycles, helps to remove the Ca2+-dependent inactivation of L-type Ca2+ channels. 3. We conclude that impairment of mitochondrial Ca2+ transport has no impact on either L-type Ca2+ currents or SR Ca2+ release at low stimulation frequencies (e.g. 0.1 Hz); however, it causes a depression of cytosolic Ca2+ transients attributable to an impaired recovery of L-type Ca2+ currents from inactivation at high stimulation frequencies (e.g. 3 Hz). The impairment of mitochondrial Ca2+ uptake and subsequent effects on Ca2+ transients at high frequencies at room temperature could be physiologically relevant since the normal heart rate of rat is around 5 Hz at body temperature. The role of mitochondria in clearing Ca2+ in the micro-domain near L-type Ca2+ channels could be impaired during high frequencies of heart beats such as in ventricular tachycardia, explaining, at least in part, the reduction of muscle contractility.
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Registered trials
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