ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Extracellular proton depression of peak and late Na⁺ current in the canine left ventricle.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Flecainide in Structural Heart Disease: Reconsidering Its Role in Contemporary Arrhythmia Management.Life (Basel, Switzerland) · 2026Review
- Impact of Impaired Kidney Function on Arrhythmia-Promoting Cardiac Ion Channel Regulation.International journal of molecular sciences · 2023Review
- Conductance Changes of NaPharmaceuticals (Basel, Switzerland) · 2023Article
- The mechanisms of potassium loss in acute myocardial ischemia: New insights from computational simulations.Frontiers in physiology · 2023Article
- Late Sodium Current of the Heart: Where Do We Stand and Where Are We Going?Pharmaceuticals (Basel, Switzerland) · 2022Review
- Late sodium current and calcium homeostasis in arrhythmogenesis.Channels (Austin, Tex.) · 2021Review
- Canine Myocytes Represent a Good Model for Human Ventricular Cells Regarding Their Electrophysiological Properties.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Late Sodium Current Inhibitors as Potential Antiarrhythmic Agents.Frontiers in pharmacology · 2020Review
- Effects of Hypoxia and Acidosis on Cardiac Electrophysiology and Hemodynamics. Is NHE-Inhibition by Cariporide Still Advantageous?Frontiers in physiology · 2020Article
- Interventricular differences in sodium current and its potential role in Brugada syndrome.Physiological reports · 2018Article
- Mechanism of Action Potential Prolongation During Metabolic Inhibition in the Whole Rabbit Heart.Frontiers in physiology · 2018Article
- Biophysical and molecular comparison of sodium current in cells isolated from canine atria and pulmonary vein.Pflugers Archiv : European journal of physiology · 2017Article
- Uncertainty quantification of fast sodium current steady-state inactivation for multi-scale models of cardiac electrophysiology.Progress in biophysics and molecular biology · 2015Review
- Dynamics of the late Na(+) current during cardiac action potential and its contribution to afterdepolarizations.Journal of molecular and cellular cardiology · 2013Article
- Developmental changes in expression and biophysics of ion channels in the canine ventricle.Journal of molecular and cellular cardiology · 2013Article
- Modulation of ventricular transient outward K⁺ current by acidosis and its effects on excitation-contraction coupling.American journal of physiology. Heart and circulatory physiology · 2013Article
- Extending the conditions of application of an inversion of the Hodgkin-Huxley gating model.Bulletin of mathematical biology · 2013Article
- Proton-dependent inhibition of the cardiac sodium channel Nav1.5 by ranolazine.Frontiers in pharmacology · 2013Article
- Physiological consequences of transient outward K+ current activation during heart failure in the canine left ventricle.Journal of molecular and cellular cardiology · 2012Article
- Extracellular proton modulation of the cardiac voltage-gated sodium channel, Nav1.5.Biophysical journal · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac ischemia reduces excitability in ventricular tissue. Acidosis (one component of ischemia) affects a number of ion currents. We examined the effects of extracellular acidosis (pH 6.6) on peak and late Na(+) current (I(Na)) in canine ventricular cells. Epicardial and endocardial myocytes were isolated, and patch-clamp techniques were used to record I(Na). Action potential recordings from left ventricular wedges exposed to acidic Tyrode solution showed a widening of the QRS complex, indicating slowing of transmural conduction. In myocytes, exposure to acidic conditions resulted in a 17.3 ± 0.9% reduction in upstroke velocity. Analysis of fast I(Na) showed that current density was similar in epicardial and endocardial cells at normal pH (68.1 ± 7.0 vs. 63.2 ± 7.1 pA/pF, respectively). Extracellular acidosis reduced the fast I(Na) magnitude by 22.7% in epicardial cells and 23.1% in endocardial cells. In addition, a significant slowing of the decay (time constant) of fast I(Na) was observed at pH 6.6. Acidosis did not affect steady-state inactivation of I(Na) or recovery from inactivation. Analysis of late I(Na) during a 500-ms pulse showed that the acidosis significantly reduced late I(Na) at 250 and 500 ms into the pulse. Using action potential clamp techniques, application of an epicardial waveform resulted in a larger late I(Na) compared with when an endocardial waveform was applied to the same cell. Acidosis caused a greater decrease in late I(Na) when an epicardial waveform was applied. These results suggest acidosis reduces both peak and late I(Na) in both cell types and contributes to the depression in cardiac excitability observed under ischemic conditions.
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Registered trials
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