title: Evaluation of remodeling in left and right ventricular myocytes from heterozygous (mRen2)27 transgenic rats.
abstract: Cardiac remodeling was assessed both in the pressure-overloaded left ventricle and in the normotensive right ventricle of hypertensive transgenic rats (mRen2)27 (TGR27). The present study combined histology, electrophysiology, molecular biology and biochemistry techniques. A significant increase in action potential (AP) duration was recorded both in right and left ventricular myocytes wheareas only in the latter ones were hypertrophic. The increase in AP duration is mainly supported by the reduction of the transient outward K current (I(to)) density since no significant modification was observed for the L-type calcium current (I(Ca,L)), the sodium-calcium exchange current (I(NCX)), the delayed rectifier current (I(K)) and the inward rectifier current (I(K1)). The lower amplitude of I(to) current was associated with a lower Kv4.3 protein expression both in right and left ventricles while Kv4.3 mRNA levels was decreased only in left ventricle. Thus, a differential ventricular remodeling takes place in the TGR27 model. The possible cause of electrical remodeling in right ventricular myocytes of TGR27 is discussed.
authors.affiliation: CNRS UMR 5123, Physiologie des Régulations Energétiques, Cellulaires et Moléculaires, Campus de la Doua, Université de Lyon 1, 69622 Villeurbanne, France.
authors.forename: Christophe
authors.initials: C
authors.lastname: Chouabe
authors.forename: Estelle
authors.initials: E
authors.lastname: Ricci
authors.forename: Mazen
authors.initials: M
authors.lastname: Kurdi
authors.forename: Claude
authors.initials: C
authors.lastname: Legrand
authors.forename: Giampiero
authors.initials: G
authors.lastname: Bricca
authors.forename: Robert
authors.initials: R
authors.lastname: Bonvallet
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D020746:Calcium Channels, L-Type / Q000378:metabolism; D004195:Disease Models, Animal; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D051379:Mice; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000502:physiology*; D011188:Potassium / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D055647:Rats, Transgenic; D012083:Renin / Q000235:genetics; D051672:Shal Potassium Channels / Q000378:metabolism; D019831:Sodium-Calcium Exchanger / Q000378:metabolism; D013997:Time Factors; D016277:Ventricular Function, Left / Q000502:physiology*; D016278:Ventricular Function, Right / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D020746:Calcium Channels, L-Type; D012333:RNA, Messenger; C473112:Ren2 protein, mouse; D051672:Shal Potassium Channels; D019831:Sodium-Calcium Exchanger; D012083:Renin; D011188:Potassium