title: Remodeling of Na,K-ATPase, and membrane fluidity after atrial fibrillation in sheep.
abstract: Atrial fibrillation (AF) is accompanied by various changes in ion channels that cause atrial electrophysiological remodeling. The enzyme Na,K-ATPase is also a major cellular mechanism for the regulation of ion homeostasis. During AF, Na,K-ATPase may be regulated by synthesis of its alpha- and beta-subunits as well as changes in membrane fluidity. To test this hypothesis, we studied the effect of pacing-induced AF in sheep on atrial Na,K-ATPase alpha- and beta-subunits and on membrane fluidity as well.
  
  
  METHODS
  A group of six sheep (AF group) was subjected to overdrive electrical stimulation of the right atrium in order to induce AF. A group of six sham operated sheep served as control. All paced sheep developed multiple episodes of sustained AF with a mean total duration of 110 min over a 2-hours period. Protein expression of Na,K-ATPase alpha- and beta-subunits in atrial microsomal membranes was assayed by Western blotting analysis. When significant changes in membrane expression were observed, transcriptional regulation was analysed by Northern blotting. Membrane fluidity was assessed on atrial microsomal fractions by anisotropy measurements using the fluorescent probe diphenylhexatriene.
  
  
  RESULTS
  Atrial fibrillation enhanced the expression of the Na,K-ATPase beta1-subunit at both membrane and mRNA levels. Anisotropy values were higher in AF group than in control group, indicating a decreased fluidity of the membranes isolated from paced sheep atria.
  
  
  CONCLUSIONS
  These data are the first evidence for an enhanced Na,K-ATPase beta1-subunit expression in membrane during AF. Membrane rigification represents a new factor of tachycardia-induced atrial remodeling.
authors.affiliation: Service de Cardiologie, Hôpital Nord, Marseille, CHU Nord, Chemin des Bourelly, 13915 Marseille Cedex 20, France. jmmaixent@gphy.campus-univ-poitiers.fr
authors.forename: Jean-Michel
authors.initials: JM
authors.lastname: Maixent
authors.forename: Marie-Josée
authors.initials: MJ
authors.lastname: Duran
authors.forename: Sandrine
authors.initials: S
authors.lastname: Pierre
authors.forename: Souad
authors.initials: S
authors.lastname: Sennoune
authors.forename: Karine
authors.initials: K
authors.lastname: Robert
authors.forename: Monique
authors.initials: M
authors.lastname: Bernard
authors.forename: Samuel
authors.initials: S
authors.lastname: Lévy
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000201:enzymology* / Q000209:etiology; D015152:Blotting, Northern; D015153:Blotting, Western; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects; D004554:Electric Countershock; D004558:Electric Stimulation; D005227:Fatty Acids / Q000378:metabolism; D005786:Gene Expression Regulation; D017136:Ion Transport / Q000502:physiology; D008560:Membrane Fluidity / Q000502:physiology*; D008861:Microsomes / Q000201:enzymology; D021122:Protein Subunits; D012756:Sheep; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics / Q000378:metabolism*; D014158:Transcription, Genetic
chemical_list: D005227:Fatty Acids; D021122:Protein Subunits; D000254:Sodium-Potassium-Exchanging ATPase