ArticleThe Journal of physiology2000
The effect of acidosis on systolic Ca2+ and sarcoplasmic reticulum calcium content in isolated rat ventricular myocytes.
Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 82 citations in OpenAlex.
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- A Simplified Langendorff-Based Method for Mouse Cardiac Myocyte Isolation.Bio-protocol · 2026Article
- CaBiomolecules · 2025Review
- Regulation of Na/Ca exchange by cytoplasmic protons modifies intracellular calcium dynamics and the cardiac response to ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Physiology of intracellular calcium buffering.Physiological reviews · 2023Review
- Impact of Impaired Kidney Function on Arrhythmia-Promoting Cardiac Ion Channel Regulation.International journal of molecular sciences · 2023Review
- Acidic environments trigger intracellular H+-sensing FAK proteins to re-balance sarcolemmal acid-base transporters and auto-regulate cardiomyocyte pH.Cardiovascular research · 2022Article
- Cardiorenal Interactions: A Review.CJC open · 2022Review
- Nitric oxide modulates cardiomyocyte pH control through a biphasic effect on sodium/hydrogen exchanger-1.Cardiovascular research · 2020Article
- Modulation of the cardiac NaCell calcium · 2020Review
- Calcium Buffering in the Heart in Health and Disease.Circulation · 2019Review
- Ups and downs of calcium in the heart.The Journal of physiology · 2018Article
- Action Potential Shortening and Impairment of Cardiac Function by Ablation ofCirculation. Arrhythmia and electrophysiology · 2017Article
- Calcium and Excitation-Contraction Coupling in the Heart.Circulation research · 2017Review
- Nuclear proton dynamics and interactions with calcium signaling.Journal of molecular and cellular cardiology · 2016Article
- Hemodynamic consequences of severe lactic acidosis in shock states: from bench to bedside.Critical care (London, England) · 2015Article
- Na⁺ ions as spatial intracellular messengers for co-ordinating Ca²⁺ signals during pH heterogeneity in cardiomyocytes.Cardiovascular research · 2015Article
- Pumping Ca2+ up H+ gradients: a Ca2(+)-H+ exchanger without a membrane.The Journal of physiology · 2014Review
- The role of CaMKII regulation of phospholamban activity in heart disease.Frontiers in pharmacology · 2014Review
- Coupled Ca2+/H+ transport by cytoplasmic buffers regulates local Ca2+ and H+ ion signaling.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated the mechanisms responsible for the changes of systolic Ca2+ that occur in voltage-clamped rat ventricular myocytes during acidosis produced by application of the weak acid butyrate (30 mM). Intracellular pH regulation was inhibited with dimethylamiloride (bicarbonate-free solution). The application of butyrate produced an intracellular acidification of 0.33 pH units. This was accompanied by a decrease in systolic Ca2+ to about 50% of control. However, within 2 min, systolic Ca2+ returned to control levels. The decrease in systolic Ca2+ was accompanied by a decrease in the Na+-Ca2+ exchange current observed on repolarisation so that the calculated Ca2+ efflux on Na+-Ca2+ exchange was less than the entry on the L-type Ca2+ current. The magnitude of the Na+-Ca2+ exchange current recovered along with systolic Ca2+ until it equalled the Ca2+ entry on the L-type Ca2+ current. From the measurement of Ca2+ fluxes, it was calculated that, during acidosis, the cell gains 121.6+/-16.2 micromol l(-1) of Ca2+. This is equal to the measured increase of sarcoplasmic reticulum (SR) calcium content obtained by applying caffeine (20 mM) and integrating the resulting Na+-Ca2+ exchange current. We conclude that the recovery of the amplitude of the systolic Ca2+ transient is due to decreased SR calcium release, resulting in reduced Ca2+ efflux from the cell leading to increased SR calcium content.
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