title: Na(+)-K(+)-ATPase alpha(2)-isoform expression in guinea pig hearts during transition from compensation to decompensation.
abstract: Disturbance in ionic gradient across sarcolemma may lead to arrhythmias. Because Na(+)-K(+)-ATPase regulates intracellular Na(+) and K(+) concentrations, and therefore intracellular Ca(2+) concentration homeostasis, our aim was to determine whether changes in the Na(+)-K(+)-ATPase alpha-isoforms in guinea pigs during transition from compensated (CLVH) to decompensated left ventricular hypertrophy (DLVH) were concomitant with arrhythmias. After 12- and 20-mo aortic stenosis, CLVH and DLVH were characterized by increased mean arterial pressure (30% and 52.7%, respectively). DLVH differed from CLVH by significantly increased end-diastolic pressure (34%), decreased sarco(endo)plasmic reticulum Ca(2+)-ATPase (-75%), and increased Na(+)/Ca(2+) exchanger (25%) mRNA levels and by the occurrence of ventricular arrhythmias. The alpha-isoform (mRNA and protein levels) was significantly lower in DLVH (2.2 +/- 0.2- and 1. 4 +/- 0.15-fold, respectively, vs. control) than in CLVH (3.5 +/- 0. 4- and 2.2 +/- 0.13-fold, respectively) and was present in sarcolemma and T tubules. Changes in the levels of alpha(1)- and alpha(3)-isoform in CLVH and DLVH appear physiologically irrelevant. We suggest that the increased level of alpha(2)-isoform in CLVH may participate in compensation, whereas its relative decrease in DLVH may enhance decompensation and arrhythmias.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale, Unité 127, Institut Fédératif de Recherche Circulation Lariboisière, Université Denis Diderot, 75475 Paris, France.
authors.forename: P
authors.initials: P
authors.lastname: Trouve
authors.forename: F
authors.initials: F
authors.lastname: Carre
authors.forename: I
authors.initials: I
authors.lastname: Belikova
authors.forename: C
authors.initials: C
authors.lastname: Leclercq
authors.forename: T
authors.initials: T
authors.lastname: Dakhli
authors.forename: L
authors.initials: L
authors.lastname: Soufir
authors.forename: I
authors.initials: I
authors.lastname: Coquard
authors.forename: J
authors.initials: J
authors.lastname: Ramirez-Gil
authors.forename: D
authors.initials: D
authors.lastname: Charlemagne
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D005260:Female; D006168:Guinea Pigs; D006333:Heart Failure; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism / Q000503:physiopathology*; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism*; D009206:Myocardium / Q000201:enzymology*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics / Q000378:metabolism*
chemical_list: D007527:Isoenzymes; D012333:RNA, Messenger; D000254:Sodium-Potassium-Exchanging ATPase