Physiological cardiac hypertrophy induced by voluntary wheel training: effects on cellular alkalinizing mechanisms

ANDRÉS MEDINA; PAULA BLANCO; ERNESTO ALEJANDRO AIELLO; LEANDRO DÍAZ ZEGARRA; ENRIQUE PORTIANSKY; ALEJANDRA YEVES; ALEJANDRO MARTÍN IBAÑEZ; VERÓNICA DE GIUSTI; IRENE ENNIS

Mar del Plata

Congreso; Reunión Anual de la Sociedad Argentina de Fisiología (SAFIS),; 2018

Sociedad Argentina de Fisiología

The Na+/HCO3- cotransport (NBC) and the cardiac Na+/H+ exchanger (NHE1) are the main alkalinizing mechanisms in cardiomyocytes. NHE1 hyperactivity is known to induce intracellular sodium overload critical for pathological cardiac cardiac hypertrophy (CH). Regarding NBC, cardiomyocytes express two isoforms: the electroneutral (NBCn1) and the electrogenic (NBCe1) that introduces one Na+ with two HCO3-. We explored NBC function in physiological CH induced by 5 weeks of voluntary wheel training in C57 mice (Results are expressed as mean ± ES, and compared by t-test). The exercise mice (Ex) runned 3.98±0.23 hs/day (4.45±0.37 Km/day) and developed CH: biventricular weight/tibial length (mg/mm): 8.61±0.23, n=16 vs. 6.65 ±0.26, n=9 and cardiomyocyte area (m2): 282±24, n=480 vs. 201±8.92, n=270, Ex and sedentary (Sed), respectively; p