REGRESSION OF LV HYPERTROPHY WITH CAPTOPRIL NORMALIZES MEMBRANE CURRENTS IN RABBITS

Recent studies indicate that regression of left ventricular hypertroph y (LVH) normalizes the in situ electrophysiological abnormalities of t he left ventricle. This study was designed to determine whether regres sion of LVH also normalizes the abnormalities of individual membrane c urrents. LVH was induced in rabbits by renal artery banding. Single ve ntricular myocytes from rabbits with LVH at 3 mo after renal artery ba nding demonstrated increased cell membrane capacitance, prolonged acti on potential duration, decreased inward rectifier K+ current density, and increased transient outward K+ current density compared with myocy tes 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 showe d persistent membrane current abnormalities. However, myocytes isolate d from LVH rabbits treated with captopril had normal cell membrane cap acitance, action potential duration, and membrane current densities. C aptopril had no direct effect on membrane currents of either control o r LVH myocytes. These data support the hypothesis that the action pote ntial prolongation and membrane current abnormalities of LVH are rever sed by regression. Normalization of membrane currents probably explain s the reduced vulnerability to ventricular arrhythmia observed in this LVH model after treatment with captopril.