PAPEL DEL INTERCAMBIADOR NA+/H+ EN LA HIPERTROFIA CARDÍACA FISIOLÓGICA

YEVES, AM; ; VILLA-ABRILLE MC; ; NOLLY, MB; ; PINILLA, OA; ; PÉREZ, NG; ; ESCUDERO, EM; ; ENNIS, IL

Santiago de Chile

Congreso; XX Annual Meeting of the International Society for Heart Research Latin American Section: Dr. Lorenzo Sazie Lecture Hall, School of Medicine, University of Chile, Santiago, Chile, October 25–26, 2012; 2012

International Society for Heart Research

Physiological cardiac hypertrophy: is the cardiac Na+/H+ exchanger (NHE1) involved? Yeves, AM; Nolly, MB; Villa-Abrille MC; Pinilla, OA; Pérez, NG; Escudero, EM; Ennis, IL  Centro de Investigaciones Cardiovasculares, UNLP-CONICET.   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 were modified. Similar results were obtained in isolated cardiomyocytes exposed to 10nM 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.