ArticleThe Journal of physiology2002
Intracellular [Na+] and Na+ pump rate in rat and rabbit ventricular myocytes.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 122 citations in OpenAlex.
- Changes in cellular CaThe Journal of physiology · 2023Article
- Nano-scale solution of the Poisson-Nernst-Planck (PNP) equations in a fraction of two neighboring cells reveals the magnitude of intercellular electrochemical waves.PLoS computational biology · 2023Article
- Heart rate changes and myocardial sodium.Physiological reports · 2022Article
- Calcium Signaling Silencing in Atrial Fibrillation: Implications for Atrial Sodium Homeostasis.International journal of molecular sciences · 2021Review
- Cardioprotection by SGLT2 Inhibitors-Does It All Come Down to NaInternational journal of molecular sciences · 2021Review
- Intracellular NaInternational journal of molecular sciences · 2021Article
- Mitochondrial CaJournal of molecular and cellular cardiology · 2021Review
- A Mathematical Model of the Mouse Atrial Myocyte With Inter-Atrial Electrophysiological Heterogeneity.Frontiers in physiology · 2020Article
- Berberine Mediated Positive Inotropic Effects on Rat HeartsFrontiers in pharmacology · 2020Article
- Pioglitazone provides beneficial effect in metabolic syndrome rats via affecting intracellular NaJournal of bioenergetics and biomembranes · 2018Article
- Myocyte [NaFrontiers in physiology · 2018Article
- Beneficial effects of leptin treatment in a setting of cardiac dysfunction induced by transverse aortic constriction in mouse.The Journal of physiology · 2017Article
- Calcium signalling silencing in atrial fibrillation.The Journal of physiology · 2017Review
- Electrophysiological Determination of Submembrane Na(+) Concentration in Cardiac Myocytes.Biophysical journal · 2016Article
- Long-Lasting Sparks: Multi-Metastability and Release Competition in the Calcium Release Unit Network.PLoS computational biology · 2016Article
- Slow [Na]i Changes and Positive Feedback Between Membrane Potential and [Ca]i Underlie Intermittent Early Afterdepolarizations and Arrhythmias.Circulation. Arrhythmia and electrophysiology · 2015Article
- Intracellular Na+ Concentration ([Na+]i) Is Elevated in Diabetic Hearts Due to Enhanced Na+-Glucose Cotransport.Journal of the American Heart Association · 2015Article
- Na+/Ca2+ exchange and Na+/K+-ATPase in the heart.The Journal of physiology · 2015Review
- Inositol-1,4,5-trisphosphate induced Ca2+ release and excitation-contraction coupling in atrial myocytes from normal and failing hearts.The Journal of physiology · 2015Article
- Ca²⁺ entry via Trpm2 is essential for cardiac myocyte bioenergetics maintenance.American journal of physiology. Heart and circulatory physiology · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Intracellular [Na+] ([Na+]i) is centrally involved in regulation of cardiac Ca2+ and contractility via Na+-Ca2+ exchange (NCX) and Na+-H+ exchange (NHX). Previous work has indicated that [Na+]i is higher in rat than rabbit ventricular myocytes. This has major functional consequences, but the reason for the higher [Na+]i in rat is unknown. Here, resting [Na+]i was measured using the fluorescent indicator SBFI, with both traditional calibration and a novel null-point method (which circumvents many limitations of prior methods). In rabbit, resting [Na+]i was 4.5 +/- 0.4 mM (traditional calibration) and 4.4 mM (null-point). Resting [Na+]i in rat was significantly higher using both the traditional calibration (11.1 +/- 0.7 mM) and the null-point approach (11.2 mM). The rate of Na+ transport by the Na+ pump was measured as a function of [Na+]i in intact cells. Rat cells exhibited a higher V(max) than rabbit (7.7 +/- 1.1 vs. 4.0 +/- 0.5 mM x min(-1)) and a higher K(m) (10.2 +/- 1.2 vs. 7.5 +/- 1.1 mM). This results in little difference in pump activity for a given [Na+]i below 10 mM, but at measured resting [Na+]i levels the pump-mediated Na+ efflux is much higher in rat. Thus, Na+ pump rate cannot explain the higher [Na+]i in rat. Resting Na+ influx rate was two to four times higher in rat, and this accounts for the higher resting [Na+]i. Using tetrodotoxin, HOE-642 and Ni2+ to block Na+ channels, NHX and NCX, respectively, we found that all three pathways may contribute to the higher resting Na+ influx in rat (albeit differentially). We conclude that resting [Na+]i is higher in rat than in rabbit, that this is caused by higher resting Na+ influx in rat and that a higher Na+,K+-ATPase pumping rate in rat is a consequence of the higher [Na+]i.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.