ArticleJournal of biomedical science2010
Nitroprusside modulates pulmonary vein arrhythmogenic activity.
Article in Journal of biomedical science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Brachial flow-mediated dilation and incident atrial fibrillation: the multi-ethnic study of atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2014Trial
- Fetal cardiomyocyte phenotype, ketone body metabolism, and mitochondrial dysfunction in the pathology of atrial fibrillation.Molecular and cellular biochemistry · 2021Review
- Brachial Flow-Mediated Dilation and Risk of Atrial Fibrillation in Older Adults: The Cardiovascular Health Study.Vascular health and risk management · 2021Article
- Endothelial dysfunction in patients with lone atrial fibrillation.ARYA atherosclerosis · 2020Article
- Mechanoelectrical feedback in pulmonary vein arrhythmogenesis: Clinical challenges and therapeutic opportunities.Journal of arrhythmia · 2020Article
- Various subtypes of phosphodiesterase inhibitors differentially regulate pulmonary vein and sinoatrial node electrical activities.Experimental and therapeutic medicine · 2020Article
- Angiotensin II Induces Automatic Activity of the Isolated Guinea Pig Pulmonary Vein Myocardium through Activation of the IP₃ Receptor and the Na⁺-CaInternational journal of molecular sciences · 2019Article
- Biomarkers and the prediction of atrial fibrillation: state of the art.Vascular health and risk management · 2016Review
- Oxidative stress in atrial fibrillation: an emerging role of NADPH oxidase.Journal of molecular and cellular cardiology · 2013Review
- Rivaroxaban modulates electrical and mechanical characteristics of left atrium.Journal of biomedical science · 2013Article
Corrections and comments
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Authors and funding
5 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPulmonary veins (PVs) are the most important sources of ectopic beats with the initiation of paroxysmal atrial fibrillation, or the foci of ectopic atrial tachycardia and focal atrial fibrillation. Elimination of nitric oxide (NO) enhances cardiac triggered activity, and NO can decrease PV arrhythmogenesis through mechano-electrical feedback. However, it is not clear whether NO may have direct electrophysiological effects on PV cardiomyocytes. This study is aimed to study the effects of nitroprusside (NO donor), on the ionic currents and arrhythmogenic activity of single cardiomyocytes from the PVs.
methodsSingle PV cardiomyocytes were isolated from the canine PVs. The action potential and ionic currents were investigated in isolated single canine PV cardiomyocytes before and after sodium nitroprusside (80 muM,) using the whole-cell patch clamp technique.
resultsNitroprusside decreased PV cardiomyocytes spontaneous beating rates from 1.7 +/- 0.3 Hz to 0.5 +/- 0.4 Hz in 9 cells (P < 0.05); suppressed delayed after depolarization in 4 (80%) of 5 PV cardiomyocytes. Nitroprusside inhibited L-type calcium currents, transient outward currents and transient inward current, but increased delayed rectified potassium currents.
conclusionNitroprusside regulates the electrical activity of PV cardiomyocytes, which suggests that NO may play a role in PV arrhythmogenesis.
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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.