ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2009
Diclofenac, a Non-steroidal Anti-inflammatory Drug, Inhibits L-type Ca Channels in Neonatal Rat Ventricular Cardiomyocytes.
Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 41 citations in OpenAlex.
- Systemic administration of analgesic buprenorphine, but not carprofen, affects cardiomyocyte contractility in rodents.Journal of molecular and cellular cardiology plus · 2025Article
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- Association of ankylosing spondylitis with cardiovascular disease: a bidirectional two-sample mendelian randomization study.Frontiers in genetics · 2024Article
- A story of the potential effect of non-steroidal anti-inflammatory drugs (NSAIDs) in Parkinson's disease: beneficial or detrimental effects.Inflammopharmacology · 2023Review
- Anti-Inflammatory and Analgesic Effects of Curcumin Nanoparticles Associated with Diclofenac Sodium in Experimental Acute Inflammation.International journal of molecular sciences · 2022Article
- Development and Challenges of Diclofenac-Based Novel Therapeutics: Targeting Cancer and Complex Diseases.Cancers · 2022Review
- Emergent Temporal Signaling in Human Trabecular Meshwork Cells: Role of TRPV4-TRPM4 Interactions.Frontiers in immunology · 2022Article
- Topical Treatments and Their Molecular/Cellular Mechanisms in Patients with Peripheral Neuropathic Pain-Narrative Review.Pharmaceutics · 2021Review
- Inhibition of Fast Nerve Conduction Produced by Analgesics and Analgesic Adjuvants-Possible Involvement in Pain Alleviation.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Microphysiological heart-liver body-on-a-chip system with a skin mimic for evaluating topical drug delivery.Lab on a chip · 2020Article
- Non-steroidal anti-inflammatory drugs and the risk of out-of-hospital cardiac arrest: a case-control study.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2019Article
- Diclofenac in the treatment of pain in patients with rheumatic diseases.Reumatologia · 2018Review
- The effects of cyclooxygenase and nitric oxide synthase inhibition on oxidative stress in isolated rat heart.Molecular and cellular biochemistry · 2013Article
- Diclofenac prolongs repolarization in ventricular muscle with impaired repolarization reserve.PloS one · 2012Article
- A Review of Topical Diclofenac Use in Musculoskeletal Disease.Pharmaceuticals (Basel, Switzerland) · 2010Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A non-steroidal anti-inflammatory drug (NSAID) has many adverse effects including cardiovascular (CV) risk. Diclofenac among the nonselective NSAIDs has the highest CV risk such as congestive heart failure, which resulted commonly from the impaired cardiac pumping due to a disrupted excitation-contraction (E-C) coupling. We investigated the effects of diclofenac on the L-type calcium channels which are essential to the E-C coupling at the level of single ventricular myocytes isolated from neonatal rat heart, using the whole-cell voltage-clamp technique. Only diclofenac of three NSAIDs, including naproxen and ibuprofen, significantly reduced inward whole cell currents. At concentrations higher than 3 microM, diclofenac inhibited reversibly the Na(+) current and did irreversibly the L-type Ca(2+) channels-mediated inward current (IC(50)=12.89+/-0.43 microM) in a dose-dependent manner. However, nifedipine, a well-known L-type channel blocker, effectively inhibited the L-type Ca(2+) currents but not the Na(+) current. Our finding may explain that diclofenac causes the CV risk by the inhibition of L-type Ca(2+) channel, leading to the impairment of E-C coupling in cardiac myocytes.
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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.