ArticleThe Journal of general physiology2011
Influence of pH on Ca²⁺ current and its control of electrical and Ca²⁺ signaling in ventricular myocytes.
Article in The Journal of general physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- Conduction Block in the Human Ischemic Myocardium: Insights from a 1D Electromechanical Model.International journal of molecular sciences · 2026Article
- Ablation of Slc26a6 Mitigates Myocardial Ischemia/Reperfusion Injury.Biomedicines · 2025Article
- A novel transgenic reporter of extracellular acidification in zebrafish elucidates skeletal muscle T-tubule pH regulation.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Article
- Computation suggests that the cell adhesion sub-proteome is enriched for sites of pH-dependence and charge burial.PloS one · 2025Article
- The calcium transient coupled to the L-type calcium current attenuates cardiac alternans.Frontiers in physiology · 2024Article
- Implications of pH and Ionic Environment in Chronic Diabetic Wounds: An Overlooked Perspective.Clinical, cosmetic and investigational dermatology · 2024Review
- Comparing the effects of chemical CaJournal of molecular and cellular cardiology · 2023Article
- The mechanisms of potassium loss in acute myocardial ischemia: New insights from computational simulations.Frontiers in physiology · 2023Article
- RNA-Seq Analyses Reveal Roles of the HVCN1 Proton Channel in Cardiac pH Homeostasis.Frontiers in cell and developmental biology · 2022Article
- Extracellular ATP-Induced Alterations in Extracellular HFrontiers in cellular neuroscience · 2021Article
- Cardiac Complications of Propionic and Other Inherited Organic Acidemias.Frontiers in cardiovascular medicine · 2020Review
- Regulation of CaCell calcium · 2019Article
- A leaky voltage sensor domain of cardiac sodium channels causes arrhythmias associated with dilated cardiomyopathy.Scientific reports · 2018Article
- A New Cardiac Channelopathy: From Clinical Phenotypes to Molecular Mechanisms Associated With NaFrontiers in cardiovascular medicine · 2018Review
- Regulation of CaJournal of molecular and cellular cardiology · 2018Article
- Mechanism of Action Potential Prolongation During Metabolic Inhibition in the Whole Rabbit Heart.Frontiers in physiology · 2018Article
- Loss-of-activity-mutation in the cardiac chloride-bicarbonate exchanger AE3 causes short QT syndrome.Nature communications · 2017Article
- Action Potential Shortening and Impairment of Cardiac Function by Ablation ofCirculation. Arrhythmia and electrophysiology · 2017Article
- Regional acidosis locally inhibits but remotely stimulates Ca2+ waves in ventricular myocytes.Cardiovascular research · 2017Article
- Metabolic inhibition reduces cardiac L-type Ca2+ channel current due to acidification caused by ATP hydrolysis.PloS one · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Modulation of L-type Ca(2+) current (I(Ca,L)) by H(+) ions in cardiac myocytes is controversial, with widely discrepant responses reported. The pH sensitivity of I(Ca,L) was investigated (whole cell voltage clamp) while measuring intracellular Ca(2+) (Ca(2+)(i)) or pH(i) (epifluorescence microscopy) in rabbit and guinea pig ventricular myocytes. Selectively reducing extracellular or intracellular pH (pH(o) 6.5 and pH(i) 6.7) had opposite effects on I(Ca,L) gating, shifting the steady-state activation and inactivation curves to the right and left, respectively, along the voltage axis. At low pH(o), this decreased I(Ca,L), whereas at low pH(i), it increased I(Ca,L) at clamp potentials negative to 0 mV, although the current decreased at more positive potentials. When Ca(2+)(i) was buffered with BAPTA, the stimulatory effect of low pH(i) was even more marked, with essentially no inhibition. We conclude that extracellular H(+) ions inhibit whereas intracellular H(+) ions can stimulate I(Ca,L). Low pH(i) and pH(o) effects on I(Ca,L) were additive, tending to cancel when appropriately combined. They persisted after inhibition of calmodulin kinase II (with KN-93). Effects are consistent with H(+) ion screening of fixed negative charge at the sarcolemma, with additional channel block by H(+)(o) and Ca(2+)(i). Action potential duration (APD) was also strongly H(+) sensitive, being shortened by low pH(o), but lengthened by low pH(i), caused mainly by H(+)-induced changes in late Ca(2+) entry through the L-type Ca(2+) channel. Kinetic analyses of pH-sensitive channel gating, when combined with whole cell modeling, successfully predicted the APD changes, plus many of the accompanying changes in Ca(2+) signaling. We conclude that the pH(i)-versus-pH(o) control of I(Ca,L) will exert a major influence on electrical and Ca(2+)-dependent signaling during acid-base disturbances in the heart.
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