Cellular Contribution to Left and Right Atrial Dysfunction in Chronic Arterial Hypertension in Pigs
Rattachement africain : at, cn, de, us, hu, be. Niveau de preuve : code pays fourni par la source.
Le résumé fourni par la source
Abstract Aims Atrial contractile dysfunction contributes to worse prognosis in hypertensive heart disease (HHD), but the role of cardiomyocyte dysfunction in atrial remodelling in HHD is not well understood. We investigated and compared cellular mechanisms of left (LA) and right atrial (RA) contractile dysfunction in pigs with HHD. Methods and results In vivo electrophysiological and magnetic resonance imaging studies were performed in control and pigs treated with 11-deoxycorticosterone acetate (DOCA)/high-salt/glucose diet (12 weeks) to induce HHD. HHD leads to significant atrial remodelling and loss of contractile function in LA and a similar trend in RA (magnetic resonance imaging). Atrial remodelling was associated with a higher inducibility of atrial fibrillation but unrelated to changes in atrial refractory period or fibrosis (histology). Reduced atrial function in DOCA pigs was related to reduced contraction amplitude of isolated LA (already at baseline) and RA myocytes (at higher frequencies) due to reduced intracellular Ca release (Fura 2-AM, field stimulation). However, Ca regulation differed in LA and RA cardiomyocytes: LA cardiomyocytes showed reduced sarcoplasmic reticulum (SR) [Ca], whereas in RA, SR [Ca] was unchanged and SR Ca2+-ATPase activity was increased. Sodium–calcium exchanger (NCX) activity was not significantly altered. We used ORM-10103 (3 μM), a specific NCX inhibitor to improve Ca availability in LA and RA cardiomyocytes from DOCA pigs. Partial inhibition of NCX increased Ca2+ transient amplitude and SR Ca in LA, but not RA cells. Conclusions In this large animal model of HHD, atrial remodelling in sinus rhythm in vivo was related to differential LA and RA cardiomyocyte dysfunction and Ca signalling. Selective acute inhibition of NCX improved Ca release in diseased LA cardiomyocytes, suggesting a potential therapeutic approach to improve atrial inotropy in HHD.
Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.
Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Cellular Contribution to Left and Right Atrial Dysfunction in Chronic Arterial Hypertension in Pigs
- Date Crossref
- 29/11/2020
- Éditeur
- Oxford University Press (OUP)
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
-
Medical University of Graz Division of Cardiology pays non établi dans la noticeUniversité ou école supérieure
-
Wenzhou Medical University pays non établi dans la noticeUniversité ou école supérieure
-
Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University pays non établi dans la noticeÉtablissement de santé
-
German Centre for Cardiovascular Research pays non établi dans la noticeStructure de recherche
-
Charité - Universitätsmedizin Berlin pays non établi dans la noticeÉtablissement de santé
-
Siemens (Austria) pays non établi dans la noticeEntreprise
-
Siemens Healthcare (United States) pays non établi dans la noticeEntreprise
-
Siemens Healthineers (Germany) pays non établi dans la noticeEntreprise
-
University of Szeged Division of Pharmacology and Pharmacotherapy pays non établi dans la noticeUniversité ou école supérieure
-
Ghent University pays non établi dans la noticeUniversité ou école supérieure
-
Deutsches Herzzentrum der Charité pays non établi dans la noticeÉtablissement de santé
-
Berlin Heart (Germany) pays non établi dans la noticeEntreprise
Division of Cardiology — Medical University of Graz, Wenzhou Medical University et Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, avec 9 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.