La regresión de la hipertrofia cardíaca inducida por inhibición del intercambiador Na+/H+ se acompaña de un efecto antiapoptótico.

GARCIARENA CD; ENNIS IL; PORTIANSKY EL; CINGOLANI HE

Buenos Aires

Congreso; XXII Latin-American & I Ibero-American Congress of Physiological Sciences; 2006

Na+/H+ exchanger (NHE-1) inhibition was demonstrated to induce the regression of cardiac hypertrophy (CH) in several experimental models and to inhibit mitochondrial death pathway in “in-vitro” experiments. We investigated the effect of chronic treatment with the NHE-1 blocker cariporide on CH and apoptosis in the hypertensive hypertrophy of the SHR. One month of treatment of cariporide (3mg/kg/day) induced the regression of CH without significant changes in blood pressure. Left ventricular weight to body weight ratio was 3.00±0.06 and 2.44±0.07 for untreated and treated SHR, respectively (p < 0.05). While a significant decrease in cardiomyocyte cross sectional area was achieved after one month of treatment (468±20 vs. 285±9 µm2, untreated and cariporide-treated SHR respectively; p < 0.05), left ventricle collagen volume fraction persisted almost the same (10.07±2.42 in untreated SHR and 8.93±1.26 % after one month of cariporide treatment; NS). The expression of Bcl-2 and Bax was assessed by Western blot analysis in the left ventricle of untreated and one month treated SHR. Chronic treatment with cariporide induced downregulation of Bcl-2 and upregulation of Bax in the left ventricular myocardium of the SHR. Therefore, the Bcl-2/Bax ratio increased (0.323±0.031 vs. 0.601±0.06, untreated and cariporide-treated SHR respectively; p < 0.05).