Selective inhibition of electrical conduction within the pulmonary veins by α1-adrenergic receptors activation in the Rat.
Action Potentials
/ physiology
Adrenergic alpha-1 Receptor Antagonists
/ metabolism
Animals
Atrial Fibrillation
/ metabolism
Electric Conductivity
Heart Atria
/ physiopathology
Heart Conduction System
/ physiopathology
Heart Rate
Male
Membrane Potentials
Myocardium
/ pathology
Myocytes, Cardiac
/ pathology
Pulmonary Veins
/ metabolism
Rats
Rats, Wistar
Receptors, Adrenergic, alpha-1
/ metabolism
Sinoatrial Node
/ physiopathology
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
25 03 2020
25 03 2020
Historique:
received:
30
12
2019
accepted:
11
03
2020
entrez:
28
3
2020
pubmed:
28
3
2020
medline:
5
1
2021
Statut:
epublish
Résumé
Pulmonary veins (PV) are involved in the pathophysiology of paroxysmal atrial fibrillation. In the rat, left atrium (LA) and PV cardiomyocytes have different reactions to α1-adrenergic receptor activation. In freely beating atria-PV preparations, we found that electrical field potential (EFP) originated from the sino-atrial node propagated through the LA and the PV. The α1-adrenergic receptor agonist cirazoline induced a progressive loss of EFP conduction in the PV whereas it was maintained in the LA. This could be reproduced in preparations electrically paced at 5 Hz in LA. During pacing at 10 Hz in the PV where high firing rate ectopic foci can occur, cirazoline stopped EFP conduction from the PV to the LA, which allowed the sino-atrial node to resume its pace-making function. Loss of conduction in the PV was associated with depolarization of the diastolic membrane potential of PV cardiomyocytes. Adenosine, which reversed the cirazoline-induced depolarization of the diastolic membrane potential of PV cardiomyocytes, restored full over-shooting action potentials and EFP conduction in the PV. In conclusion, selective activation of α1-adrenergic receptors results in the abolition of electrical conduction within the PV. These results highlight a potentially novel pharmacological approach to treat paroxysmal atrial fibrillation by targeting directly the PV myocardium.
Identifiants
pubmed: 32214185
doi: 10.1038/s41598-020-62349-5
pii: 10.1038/s41598-020-62349-5
pmc: PMC7096464
doi:
Substances chimiques
Adrenergic alpha-1 Receptor Antagonists
0
Receptors, Adrenergic, alpha-1
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
5390Références
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