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Investigating the TASK1 potassium channel in equine atrial myocardium as a potential treatment target for atrial fibrillation.
Abstract: Atrial fibrillation (AF) is the most common clinically relevant arrhythmia in horses, with limited pharmacological treatment options in both veterinary and human medicine. TASK1 potassium channels represent a promising atrial-selective antiarrhythmic target, but their relevance in horses has not been established. To characterize equine TASK1 (eqTASK1) channels regarding structural conservation, electrophysiological function, pharmacological sensitivity, cardiac expression pattern and in vivo electrophysiological effects of TASK1 inhibition. Methods: Sixteen horses killed for non-cardiovascular reasons, of which 10 horses used for tissue harvesting and six horses for in vivo testing. Functional and pharmacological properties of eq TASK1 and human (hTASK1) channels were assessed in Xenopus laevis oocytes using two-electrode voltage clamp recordings. Cardiac expression of eqTASK1 was analysed by qRT-PCR and immunoblotting, while in vivo electrophysiological studies were performed in anaesthetized horses before and after intravenous ketodoxapram administration. Results: EqTASK1 and h TASK1 channels demonstrated high structural conservation, comparable potassium-selective background currents and preserved pharmacological sensitivity with species-dependent differences in potency. EqTASK1 expression was strongly enriched in atrial and nodal tissue, whereas ventricular expression was minimal. In vivo administration of ketodoxapram significantly prolonged atrial effective refractory periods from 275 ± 54 to 418 ± 94 ms without significant changes in heart rate or atrioventricular conduction parameters. Conclusions: EqTASK1 channels are highly conserved with human orthologs and display pronounced atrial-predominant cardiac expression. In vivo TASK1 inhibition prolongs atrial refractoriness in horses, supporting TASK1 as a translational atrial-selective antiarrhythmic target in both human and veterinary medicine.
© 2026 British Pharmacological Society.
Publication Date: 2026-10-24 PubMed ID: 42920365DOI: 10.1111/bph.70703Google Scholar: Lookup The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
Summary
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Overview
- This research investigates the TASK1 potassium channel in horse heart tissue to explore its potential as a treatment target for atrial fibrillation (AF), a common heart rhythm disorder in horses and humans.
- The study characterizes the structural, functional, and pharmacological properties of equine TASK1 channels and evaluates the effect of TASK1 inhibition on heart electrophysiology in live horses.
Background and Significance
- Atrial fibrillation (AF) is a prevalent and clinically significant arrhythmia in horses, with limited effective drug treatments available.
- TASK1 potassium channels are promising targets for antiarrhythmic therapy because they are selective to atrial heart tissue, which may help avoid unwanted effects on the ventricles.
- Prior to this study, the importance and characteristics of TASK1 channels in horses had not been fully established.
Objectives
- To characterize the equine TASK1 (eqTASK1) potassium channels in terms of their structural similarity to human TASK1 channels.
- To assess the electrophysiological function and pharmacological sensitivity of eqTASK1 channels.
- To determine the cardiac tissue expression pattern of eqTASK1 channels in horses.
- To investigate the effects of TASK1 channel inhibition on heart electrophysiology in live horses.
Methods
- Sample Sources:
- 16 horses euthanized for non-cardiac reasons were studied; 10 for tissue analysis and 6 for live electrophysiological testing.
- Functional and Pharmacological Testing:
- EqTASK1 and human TASK1 (hTASK1) channels were expressed in Xenopus laevis oocytes for electrophysiological recordings using two-electrode voltage clamp techniques.
- The potassium background currents and drug sensitivity were compared between species.
- Tissue Expression Analysis:
- Quantitative reverse transcription PCR (qRT-PCR) and immunoblotting were used to measure TASK1 mRNA and protein levels in different heart regions (atria, ventricles, and nodal tissues).
- In Vivo Electrophysiological Study:
- Six anesthetized horses underwent electrophysiological measurements before and after intravenous administration of ketodoxapram, a TASK1 inhibitor.
- Parameters measured included atrial effective refractory period, heart rate, and atrioventricular conduction metrics.
Results
- Structural Conservation:
- EqTASK1 channels showed high sequence and structural similarity to human TASK1 channels, indicating conserved function across species.
- Electrophysiological Function:
- Both eqTASK1 and hTASK1 produced comparable potassium-selective background currents upon voltage clamping.
- Pharmacological Sensitivity:
- EqTASK1 channels responded to TASK1 inhibitors with preserved pharmacological sensitivity, although there were species-specific differences in drug potency.
- Cardiac Expression Pattern:
- EqTASK1 expression was highly enriched in atrial myocardium and nodal tissues, with minimal presence in ventricular myocardium.
- In Vivo Effects of TASK1 Inhibition:
- Administration of ketodoxapram significantly prolonged the atrial effective refractory period (from about 275 ms to 418 ms), a change beneficial for preventing arrhythmias.
- No significant alterations were observed in heart rate or atrioventricular conduction, suggesting atrial selectivity and minimal side effects.
Conclusions
- Equine TASK1 channels are highly conserved and functionally similar to human TASK1 channels.
- The expression of TASK1 is predominantly atrial, supporting its role as an atrial-selective target.
- In vivo inhibition of TASK1 channels in horses prolongs atrial refractoriness without affecting heart rate or conduction, highlighting its potential as a safe and effective therapeutic target for AF.
- This research supports the translational relevance of TASK1 as an atrial-specific antiarrhythmic target for both human and veterinary medicine.
Implications and Future Directions
- TASK1 inhibitors like ketodoxapram may represent a new class of atrial-selective antiarrhythmic drugs with fewer side effects.
- Further research could focus on clinical trials in horses with AF to confirm efficacy and safety.
- The conserved nature of TASK1 suggests potential applicability of TASK1-targeted therapies across species, benefiting both veterinary and human cardiac arrhythmia treatments.
Cite This Article
APA
Verhaeghe LM, Jávorszky N, Kraft M, Wiedmann F, Weitkamp FM, Decloedt A, Van Steenkiste G, van Loon G, Schmidt C.
(2026).
Investigating the TASK1 potassium channel in equine atrial myocardium as a potential treatment target for atrial fibrillation.
Br J Pharmacol.
https://doi.org/10.1111/bph.70703 Publication
Researcher Affiliations
- Equine Cardioteam Ghent, Department of Internal Medicine, Reproduction and Population Medicine, Faculty of Veterinary Medicine, Ghent University, Ghent, Belgium.
- Department of Cardiology, Angiology and Pneumology, University Hospital Heidelberg, Heidelberg, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg/Mannheim, University of Heidelberg, Heidelberg, Germany.
- Department of Urology, Jahn Ferenc South-Pest Hospital, Budapest, Hungary.
- Department of Cardiology, Angiology and Pneumology, University Hospital Heidelberg, Heidelberg, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg/Mannheim, University of Heidelberg, Heidelberg, Germany.
- Department of Cardiology, Angiology and Pneumology, University Hospital Heidelberg, Heidelberg, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg/Mannheim, University of Heidelberg, Heidelberg, Germany.
- Department of Cardiology and Pneumology, University Medical Center Göttingen, Göttingen, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Lower Saxony, University of Goettingen, Goettingen, Germany.
- Department of Cardiology and Pneumology, University Medical Center Göttingen, Göttingen, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Lower Saxony, University of Goettingen, Goettingen, Germany.
- Equine Cardioteam Ghent, Department of Internal Medicine, Reproduction and Population Medicine, Faculty of Veterinary Medicine, Ghent University, Ghent, Belgium.
- Equine Cardioteam Ghent, Department of Internal Medicine, Reproduction and Population Medicine, Faculty of Veterinary Medicine, Ghent University, Ghent, Belgium.
- Equine Cardioteam Ghent, Department of Internal Medicine, Reproduction and Population Medicine, Faculty of Veterinary Medicine, Ghent University, Ghent, Belgium.
- Department of Cardiology, Angiology and Pneumology, University Hospital Heidelberg, Heidelberg, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg/Mannheim, University of Heidelberg, Heidelberg, Germany.
- Department of Cardiology and Pneumology, University Medical Center Göttingen, Göttingen, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Lower Saxony, University of Goettingen, Goettingen, Germany.
Grant Funding
- EKFS Clinician-Scientist Professorship / Else Kröner-Fresenius-Stiftung
- CRC1550 / Deutsche Forschungsgemeinschaft
- 464424253 / German Research Foundation (DFG)
- 81X4500125 / German Centre for Cardiovascular Research (DZHK)
- 81X4500132 / German Centre for Cardiovascular Research (DZHK)
- 81X4500124 / German Centre for Cardiovascular Research (DZHK)
- 81X4500117 / German Centre for Cardiovascular Research (DZHK)
- 81X4300142 / German Centre for Cardiovascular Research (DZHK)
- German Cardiac Society (DGK)
- German Heart Foundation/German Foundation of Heart Research
- Joachim-Herz Foundation
- Else-Kröner Fresenius Foundation
- Zukunft. Niedersachsen
- Grayson-Jockey Club Research Foundation
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