CENTRO DE INVESTIGACIONES CARDIOVASCULARES "DR. HORACIO EUGENIO CINGOLANI"
Unidad Ejecutora - UE
congresos y reuniones científicas
Physiological cardiac hypertrophy: Is the cardiac Na+/H+ exchanger (NHE-1) involved?
ALEJANDRA M. YEVES; NOLLY, MARIELA B; MARÍA C. VILLA-ABRILLE; OSCAR ANDRÉS PINILLA; PEREZ NG; EDUARDO M. ESCUDERO; ENNIS I
Congreso; XX Annual Meeting of the International Society for Heart Research Latin American Section; 2012
Physiological cardiac hypertrophy: Is the cardiac Na+/H+ exchanger (NHE1) involved? A.M. Yeves, M.B. Nolly, M.C. Villa-Abrille, O.A. Pinilla, N.G. Pérez, E.M. Escudero, I.L. Ennis Centro de Investigaciones Cardiovasculares, UNLP-CONICET, Argentina Physiological cardiac hypertrophy (CH) is an adaptive response to increased workload induced by training or pregnancy while pathological CH is due to pathological overload (i.e. hypertension) and usually evolves to arrhythmias and heart failure. We aimed to further elucidate differences in the underlying pathway in both types of CH, specially focusing in the role played by the NHE1. Physiological CH [biventricular weight/tibia length: 22.0±0.3 vs. 24.3±0.7 mg/mm; sedentary (S) and trained (T)] was induced in rats by swimming (90 min/day, 12 weeks). No differences in systolic function but a lower stiffness correlated with decreased collagen deposition [1.7± 0.05 (S) vs. 1.4±0.09 (N)] were detected in T. While activation of PI3-K/AKT signaling [PI3-K expression: 153±18 (T) vs. 100±10 (S); and P-AKT: 134±10 (T) vs. 100±5 (S) %]; was detected in the hypertrophied myocardium neither NHE1 [100±8.5 (S) vs. 95±6.7 % (N)] nor BNP (100±15 vs. 99±15 %) expression was modified. Similar results were obtained in isolated cardiomyocytes exposed to 10 nM IGF1. IGF1 increased myocyte area (111±2 vs. 100±2 %) and protein/DNA (109±1.8 vs. 100±1.5 %), effects not abolished by NHE1 inhibition. IGF1 also increased P-AKT (100±5.9 vs. 122± 5.7; control and IGF1) but did not affect NHE1 activity (JH+ at pHi 6.8: 2.1±0.2 vs. 1.8±0.2; control and IGF1). These results suggest that the NHE1; a critical mediator of pathological CH, is not involved in physiological CH.