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Cited by 130Mitochondrial Function and PathologyCardiac Ischemia and ReperfusionCardiovascular Function and Risk Factors

Intracellular Ca 2+ Increases the Mitochondrial NADH Concentration During Elevated Work in Intact Cardiac Muscle

Brandes, Rolf, Bers, Donald M.·1997·Circulation Research
DOI 10.1161/01.res.80.1.82
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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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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
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1997-01
Volume
80
Issue
1
Pages
82-87
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
DOI
10.1161/01.res.80.1.82
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 › Pathology and Forensic 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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