Increased Na+/Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats.

JESICA RODRIGUEZ; MATILDE SAID; J. OMAR VELEZ RUEDA; MARGARITA SALAS; ROMINA BECERRA; MARIANO N. DI CARLO; LETICIA VITTONE; GUSTAVO RINALDI; ENRIQUE L. PORTIANSKY; CECILIA MUNDIÑA - WEILENMANN; JULIETA PALOMEQUE; ALICIA MATTIAZZI

PLOS ONE

PUBLIC LIBRARY SCIENCE

Lugar: San Francisco; Año: 2014 vol. 9

1932-6203

Spontaneously hypertensive rat (SHR) constitutes a genetic model widely used to study the natural evolution of hypertensive heart disease. Ca2+ -handling alterations are known to occur in SHR. However, the putative modifications of Ca2+ -handling proteins during the progression to heart failure (HF) are not well established. Moreover, the role of apoptosisin SHR is controversial. We investigated intracellular Ca2+, Ca2+ -handling proteins and apoptosis in SHR vs. control Wistar rats (W) from 3 to 15 months (mo). Changes associated with the transition to HF (i.e. lung edema and decrease in midwall fractional shortening), occurred at 15 mo in 38% of SHR (SHRF). In SHRF, twitch and caffeine-induced Ca2+ transients, significantly decreased relative to 6/9 mo and 15 mo without HF signs. This decrease occurred in association with a decrease in the time constant of caffeine-Ca2+ transient decay and an increase in Na+ /Ca2+ exchanger (NCX) abundance (p