The DOI matches its Crossref record; 31 of the 32 references it cites were found in a registry or an index.
Intracellular Ca 2+ Increases the Mitochondrial NADH Concentration During Elevated Work in Intact Cardiac Muscle
Abstract
It is not clear how mitochondrial energy production is regulated in intact tissue when energy consumption suddenly changes. Whereas mitochondrial [NADH] ([NADH] m ) may regulate cellular respiration rate and energetic state, it is not clear how [NADH] m itself is controlled during increased work in vivo. We have varied work and [Ca 2+ ] in intact cardiac muscle while assessing [NADH] m using fluorescence spectroscopy. When increased work was accompanied by increasing average [Ca 2+ ] c (by increasing [Ca 2+ ] o or pacing frequency), [NADH] m initially fell and subsequently recovered to a new steady state level. Upon reduction of work, [NADH] m overshot and then returned to control levels. In contrast, when work was increased without increasing average [Ca 2+ ] c (by increasing sarcomere length), [NADH] m fell similarly, but no recovery or overshoot was observed. This Ca 2+ -dependent recovery and overshoot may be attributed to Ca 2+ -dependent stimulation of mitochondrial dehydrogenases. We conclude that the immediate initial increase in respiration rate upon elevation of work is not activated by increased [NADH] m (since [NADH] m rapidly fell) or by [Ca 2+ ] c (since work could also be increased at constant [Ca 2+ ] c ). However, during sustained high work, a Ca 2+ -dependent mechanism causes slow recovery of [NADH] m toward control values. This demonstrates a Ca 2+ -dependent feed-forward control mechanism of cellular energetics in cardiac muscle during increased work.
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“A small class of “uncoupling” proteins, called UCPs 1–4, are believed to induce an inward proton “leak” in charged mitochondria (49, 55, 176, 300).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [49]
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“Its time course does not exhibit the “on-undershoot” observed in isolated trabeculae (5), because the activation of NADH production is not significantly delayed in relation to the activation of NADH consumption (see DISCUSSION).”
BackgroundDynamic adaptation of cardiac oxidative phosphorylation is not mediated by simple feedback control
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Metadata
- Authors
- Brandes, R., & Bers, D. M.
- Affiliations
- the Department of Physiology, Loyola University Chicago, School of Medicine, Maywood, Ill. E-mail rbrande@luc.edu
- Loyola University Chicago (US)
- ORCID
- Bers, Donald M.
- Venue
- Circulation Research
- Published
- 1997-01
- Volume
- 80
- Issue
- 1
- Pages
- 82-87
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W1979697035
- Cited by
- 130
- References
- 32
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 2 · 2023: 5 · 2022: 2 · 2021: 4 · 2020: 2 · 2019: 4 · 2018: 6 · 2017: 5 · 2016: 5 · 2015: 8 · 2014: 3 · 2013: 5 · 2012: 4
- FWCI
- 2.37
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01hl052478-05)
- National Heart, Lung, and Blood Institute (HL52478, HL30077)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Keywords
- intracellular calcium, mitochondrial NADH, myocardium, mitochondrial respiration, energy metabolism, sarcomere length, pacing rate, mitochondrial dehydrogenases, feedforward control, NADH fluorescence
- MeSH terms
- Animals, Calcium, Energy Metabolism, Intracellular Membranes, Kinetics, Male, Mitochondria, NAD, Osmolar Concentration, Papillary Muscles, Rats, Inbred Strains, Temperature, Rats
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