title: Regression of LV hypertrophy with captopril normalizes membrane currents in rabbits.
abstract: Recent studies indicate that regression of left ventricular hypertrophy (LVH) normalizes the in situ electrophysiological abnormalities of the left ventricle. This study was designed to determine whether regression of LVH also normalizes the abnormalities of individual membrane currents. LVH was induced in rabbits by renal artery banding. Single ventricular myocytes from rabbits with LVH at 3 mo after renal artery banding demonstrated increased cell membrane capacitance, prolonged action potential duration, decreased inward rectifier K+ current density, and increased transient outward K+ current density compared with myocytes from age-matched controls. Additional rabbits were randomized at 3 mo after banding to treatment with either vehicle or captopril for an additional 3 mo. Myocytes from LVH rabbits treated with vehicle showed persistent membrane current abnormalities. However, myocytes isolated from LVH rabbits treated with captopril had normal cell membrane capacitance, action potential duration, and membrane current densities. Captopril had no direct effect on membrane currents of either control or LVH myocytes. These data support the hypothesis that the action potential prolongation and membrane current abnormalities of LVH are reversed by regression. Normalization of membrane currents probably explains the reduced vulnerability to ventricular arrhythmia observed in this LVH model after treatment with captopril.
authors.affiliation: Cardiovascular Division, The Lankenau Hospital and Medical Research Center, Wynnewood 19096, USA.
authors.forename: S J
authors.initials: SJ
authors.lastname: Rials
authors.forename: X
authors.initials: X
authors.lastname: Xu
authors.forename: Y
authors.initials: Y
authors.lastname: Wu
authors.forename: R A
authors.initials: RA
authors.lastname: Marinchak
authors.forename: P R
authors.initials: PR
authors.lastname: Kowey
mesh_terms: D000200:Action Potentials / Q000187:drug effects* / Q000502:physiology; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D002216:Captopril / Q000627:therapeutic use*; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D006321:Heart / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000503:physiopathology*; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009392:Nephrectomy; D009929:Organ Size / Q000187:drug effects; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D024661:Potassium Channels, Inwardly Rectifying; D011817:Rabbits; D012077:Renal Artery / Q000502:physiology; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000502:physiology
chemical_list: D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D002216:Captopril