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Na+/H+ Exchanger Inhibition Induces
Regression of Cardiac Hypertrophy in
the Spontaneously Hypertensive
Rat (SHR)

Camilión de Hurtado, María C.; Pérez, Néstor G.;
Portiansky, Enrique; Cingolani, Horacio E.

Centro de Investigaciones Cardiovasculares,
Facultad de Ciencias Médicas,
La Plata, Argentina

   We previously showed that enalapril treatment induced the regression of cardiac hypertrophy (CH) together with the normalization of myocardial exchanger (NHE) hyperactivity in SHR (Hypertension. 1998;31:961). The objective of this report was to study the effect of chronic inhibition of the NHE1 (main NHE isoNa+/H+form expressed in cardiac tissue) on the CH of SHR. Male, 5-mo old SHR were treated during 2 months with cariporide (CARI) in the drinking water at the dosage of 0.3 (low dose) or 3.0 (high dose) mg/Kg/day. Body weight (BW) and systolic blood pressure (SBP) were monitored weekly during the treatment. CH (assessed by the heart weight (mg)/BW (g) ratio) decreased from 3.54 ± 0.09 (n=8) to 3.15 ± 0.11 (n=8) and 2.99 ± 0.05 (n=4, P<0.05, ANOVA) after treatment with low or high dose of CARI, respectively. Cardiomyocyte size decreased from 440.5 ± 38.7 in untreated SHR (n=4) to 202.8 ± 13.5 ?m2 in CARI (n=4), value not different to that found in the myocardium of normotensive rats (285.9 ± 20.3, n=4). CARI (either the low or high dose) induced only a small decrease in SBP by 8.0 ± 1.5 mmHg. The results, therefore, clearly demonstrate the ability of prolonged inhibition of NHE1 activity to promote the regression of CH in SHR and may contribute to a further understanding of the role of the NHE1 activity in the cardiac growth



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2nd Virtual Congress of Cardiology

Dr. Florencio Garófalo
Steering Committee
Dr. Raúl Bretal
Scientific Committee
Dr. Armando Pacher
Technical Committee - CETIFAC

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