ArticleJournal of molecular and cellular cardiology2011
Angiotensin II induces afterdepolarizations via reactive oxygen species and calmodulin kinase II signaling.
Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 63 citations in OpenAlex.
- Role of NADPH oxidase 2-derived reactive oxygen species in cardiac electrophysiological disorders.Channels (Austin, Tex.) · 2026Review
- Hyperglycaemia-induced reactive oxygen species production in cardiac ventricular myocytes differs among mammals.The Journal of physiology · 2026Article
- Anti-Arrhythmic Effects of Heart Failure Guideline-Directed Medical Therapy and Their Role in the Prevention of Sudden Cardiac Death: From Beta-Blockers to Sodium-Glucose Cotransporter 2 Inhibitors and Beyond.Journal of clinical medicine · 2024Review
- NADPH Oxidases and Oxidative Stress in the Pathogenesis of Atrial Fibrillation.Antioxidants (Basel, Switzerland) · 2023Review
- Impact of Impaired Kidney Function on Arrhythmia-Promoting Cardiac Ion Channel Regulation.International journal of molecular sciences · 2023Review
- Review
- Ranolazine: An Old Drug with Emerging Potential; Lessons from Pre-Clinical and Clinical Investigations for Possible Repositioning.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Effective Accentuation of Voltage-Gated Sodium Current Caused by Apocynin (4'-Hydroxy-3'-methoxyacetophenone), a Known NADPH-Oxidase Inhibitor.Biomedicines · 2021Article
- Cardiac adaptation and cardioprotection against arrhythmias and ischemia-reperfusion injury in mammalian hibernators.Pflugers Archiv : European journal of physiology · 2021Review
- Activation of TRPC (Transient Receptor Potential Canonical) Channel Currents in Iron Overloaded Cardiac Myocytes.Circulation. Arrhythmia and electrophysiology · 2021Article
- CaMKII Inhibition is a Novel Therapeutic Strategy to Prevent Diabetic Cardiomyopathy.Frontiers in pharmacology · 2021Review
- Iron Overload, Oxidative Stress and Calcium Mishandling in Cardiomyocytes: Role of the Mitochondrial Permeability Transition Pore.Antioxidants (Basel, Switzerland) · 2020Article
- Thioridazine Induces Cardiotoxicity via Reactive Oxygen Species-Mediated hERG Channel Deficiency and L-Type Calcium Channel Activation.Oxidative medicine and cellular longevity · 2020Article
- The transient receptor potential melastatin 4 channel inhibitor 9-phenanthrol modulates cardiac sodium channel.British journal of pharmacology · 2018Article
- Loss of p21-activated kinase 1 (Pak1) promotes atrial arrhythmic activity.Heart rhythm · 2018Article
- CaMKIIδ-mediated inflammatory gene expression and inflammasome activation in cardiomyocytes initiate inflammation and induce fibrosis.JCI insight · 2018Article
- Epac2-Rap1 Signaling Regulates Reactive Oxygen Species Production and Susceptibility to Cardiac Arrhythmias.Antioxidants & redox signaling · 2017Article
- CaMKII: The molecular villain that aggravates cardiovascular disease.Experimental and therapeutic medicine · 2017Article
- Angiotensin II Induced Cardiac Dysfunction on a Chip.PloS one · 2016Article
- Activation of M3 cholinoceptors attenuates vascular injury after ischaemia/reperfusion by inhibiting the Ca2+/calmodulin-dependent protein kinase II pathway.British journal of pharmacology · 2015Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Renin-angiotensin system inhibitors significantly reduce the incidence of arrhythmias. However, the underlying mechanism(s) is not well understood. We aim to test the hypothesis that angiotensin II (Ang II) induces early afterdepolarizations (EADs) and triggered activities (TAs) via the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-ROS-calmodulin kinase II (CaMKII) pathway. ROS production was analyzed in the isolated rabbit myocytes loaded with ROS dye. Ang II (1-2 μM) increased ROS fluorescence in myocytes, which was abolished by Ang II type 1 receptor blocker losartan, NADPH oxidase inhibitor apocynin, and antioxidant MnTMPyP, respectively. Action potentials were recorded using the perforated patch-clamp technique. EADs emerged in 27 out of 41 (66%) cells at 15.8 ± 1.6 min after Ang II (1-2 μM) perfusion. Ang II-induced EADs were eliminated by losartan, apocynin, or trolox. The CaMKII inhibitor KN-93 (n=6) and inhibitory peptide (AIP) (n=4) also suppressed Ang II-induced EADs, whereas the inactive analogue KN-92 did not. Nifedipine, a blocker of L-type Ca current (I(Ca)(2+)(,L)), or ranolazine, an inhibitor of late Na current (I(Na)(+)), abolished Ang II-induced EADs. The effects of Ang II on major membrane currents were evaluated using voltage clamp. While Ang II at same concentrations had no significant effect on total outward K(+) current, it enhanced I(Ca.L) and late I(Na), which were attenuated by losartan, apocynin, trolox, or KN-93. We conclude that Ang II induces EADs via intracellular ROS production through NADPH oxidase, activation of CaMKII, and enhancement of I(Ca,L) and late I(Na). These results provide evidence supporting a link between renin-angiotensin system and cardiac arrhythmias.
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