ArticlePflugers Archiv : European journal of physiology2012
Persistent sodium current and Na+/H+ exchange contributes to the augmentation of the reverse Na+/Ca2+ exchange during hypoxia or acute ischemia in ventricular myocytes.
Article in Pflugers Archiv : European journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 45 citations in OpenAlex.
- 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
- Cardioprotection by SGLT2 Inhibitors-Does It All Come Down to NaInternational journal of molecular sciences · 2021Review
- Dual Mechanisms of Cardiac Action Potential Prolongation by 4-Oxo-Nonenal Increasing the Risk of Arrhythmia; Late NaAntioxidants (Basel, Switzerland) · 2021Article
- Late Sodium Current Inhibitors as Potential Antiarrhythmic Agents.Frontiers in pharmacology · 2020Review
- Curcumin, a Multi-Ion Channel Blocker That Preferentially Blocks Late NaFrontiers in physiology · 2020Article
- Ischemia Enhances the Acute Stretch-Induced Increase in Calcium Spark Rate in Ventricular Myocytes.Frontiers in physiology · 2020Article
- Late sodium current associated cardiac electrophysiological and mechanical dysfunction.Pflugers Archiv : European journal of physiology · 2018Review
- Barbaloin inhibits ventricular arrhythmias in rabbits by modulating voltage-gated ion channels.Acta pharmacologica Sinica · 2018Article
- Na/K pump inactivation, subsarcolemmal Na measurements, and cytoplasmic ion turnover kinetics contradict restricted Na spaces in murine cardiac myocytes.The Journal of general physiology · 2017Article
- Icariin, a Novel Blocker of Sodium and Calcium Channels, Eliminates Early and Delayed Afterdepolarizations, As Well As Triggered Activity, in Rabbit Cardiomyocytes.Frontiers in physiology · 2017Article
- Essential role of Na+/Ca2+ exchanger 1 in smoking-induced growth and migration of esophageal squamous cell carcinoma.Oncotarget · 2016Article
- Ketamine attenuates the Na+-dependent Ca2+ overload in rabbit ventricular myocytes in vitro by inhibiting late Na+ and L-type Ca2+ currents.Acta pharmacologica Sinica · 2015Article
- p21-Activated kinase1 (Pak1) is a negative regulator of NADPH-oxidase 2 in ventricular myocytes.Journal of molecular and cellular cardiology · 2014Article
- Nav 1.5 mutations linked to dilated cardiomyopathy phenotypes: Is the gating pore current the missing link?Channels (Austin, Tex.) · 2014Article
- A new method to detect rapid oxygen changes around cells: how quickly do calcium channels sense oxygen in cardiomyocytes?Journal of applied physiology (Bethesda, Md. : 1985) · 2013Article
- Anandamide reduces intracellular Ca2+ concentration through suppression of Na+/Ca2+ exchanger current in rat cardiac myocytes.PloS one · 2013Article
- Sodium overload due to a persistent current that attenuates the arrhythmogenic potential of a novel LQT3 mutation.Frontiers in pharmacology · 2013Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The increases in persistent sodium currents (I (Na.P)) and Na(+)/H(+) exchange (NHE) causes intracellular Ca(2+) overload. The objective of this study was to determine the contribution of I (Na.P) and NHE on the hypoxia- or acute ischemia-induced increase in the reverse Na(+)/Ca(2+) exchange current (HIR- or AIR-I (NCX)). I (Na.P) and I (NCX) in rabbit ventricular myocytes were recorded during hypoxia or acute ischemia, combination of acidosis (pH values were 6.0 intracellularly and 6.8 extracellularly) and hypoxia, using whole-cell patch-clamp techniques. The results indicate that (1) under hypoxic condition, the augmentation of both HIR-I (NCX) and I (Na.P) was inhibited by TTX (2 to 8 μM) in a concentration-dependent manner. The inhibitions of I (Na,P) and HIR-I (NCX) reached maximum in the presence of either 4 μM TTX or 10 μM KR-32568 (a NHE inhibitor), respectively. The maximal inhibitions of HIR-I (NCX) by 4 μM TTX and 10 μM KR-32568 were 72.54% and 16.89%, respectively. (2) Administration of 2 μM TTX and 10 μM KR-32568 in either order in the same cells decreased HIR-I (NCX) by 64.83% and 16.94%, respectively. (3) I (Na.P) and the reverse I (NCX) were augmented during acute ischemia. TTX (4 μM) and KR-32568 (10 μM) reduced AIR-I (NCX) by 73.39% and 24.13%, respectively. (4) Under normoxic condition, veratridine (20 μM) significantly increased I (Na.P) and the reverse I (NCX), which was reversed by 4 μM TTX. In conclusion, during hypoxia or acute ischemia, both increased I (Na.P) and NHE contribute to the HIR- or AIR-I (NCX) with the former playing a major role comparing with the latter.
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