ArticleNature communications2018
Neurokinin-3 receptor activation selectively prolongs atrial refractoriness by inhibition of a background K
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Heart Failure and Atrial Fibrillation in Women: Pathophysiological Links, Clinical Challenges, and Therapeutic Perspectives.Medicina (Kaunas, Lithuania) · 2026Review
- Unravelling Sex Disparities in the Pathophysiology of Atrial Fibrillation: Review of the Current Evidence.Journal of cardiovascular electrophysiology · 2025Review
- The Antidepressant Paroxetine Reduces the Cardiac Sodium Current.International journal of molecular sciences · 2023Article
- Tachykinin receptor 3 in the lateral habenula alleviates pain and anxiety comorbidity in mice.Frontiers in immunology · 2023Article
- Small conductance calcium activated KInternational journal of cardiology. Heart & vasculature · 2021Article
- Absence of Functional NaCardiovascular drugs and therapy · 2019Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cardiac autonomic nervous system (ANS) controls normal atrial electrical function. The cardiac ANS produces various neuropeptides, among which the neurokinins, whose actions on atrial electrophysiology are largely unknown. We here demonstrate that the neurokinin substance-P (Sub-P) activates a neurokinin-3 receptor (NK-3R) in rabbit, prolonging action potential (AP) duration through inhibition of a background potassium current. In contrast, ventricular AP duration was unaffected by NK-3R activation. NK-3R stimulation lengthened atrial repolarization in intact rabbit hearts and consequently suppressed arrhythmia duration and occurrence in a rabbit isolated heart model of atrial fibrillation (AF). In human atrial appendages, the phenomenon of NK-3R mediated lengthening of atrial repolarization was also observed. Our findings thus uncover a pathway to selectively modulate atrial AP duration by activation of a hitherto unidentified neurokinin-3 receptor in the membrane of atrial myocytes. NK-3R stimulation may therefore represent an anti-arrhythmic concept to suppress re-entry-based atrial tachyarrhythmias, including AF.
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Registered trials
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