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Regression of Cardiac Hypertrophy
by Na+/H+ Exchanger Blockade in the
Spontaneously Hypertensive Rat

Camilión de Hurtado, MC;
Pérez, NG; Cingolani, HE

Centro de Investigaciones Cardiovasculares. Facultad de Ciencias
Médicas, Universidad Nacional de La Plata, La Plata, Argentina

Na+/H+ exchanger (NHE) activity has been shown enhanced in a substantial variety of cell types obtained from essential hypertensive patients and animals with experimental forms of hypertension. NHE hyperactivity was detected in the hypertrophied heart of the spontaneously hypertensive rat (SHR), but it is still unknown whether this hyperactivity is an epiphenomenon or has a causal link with cardiac hypertrophy (CH). To get further insight in this subject, SHR were treated for 30 days either with HOE 642 (specific NHE-1 inhibitor), Enalapril (E) or Nifedipine (N). Drugs were given in the drinking water at a dosage of (mg/kg/day) 0.3 of HOE 642, 20 of E or 10 of N. Arterial pressure (AP) was measured weekly and at the end of the treatment the rats were killed, the heart weight to body weight ratio (HI) determined, and papillary muscles (pm) isolated to measure intracellular pH (pHi) by epifluorescence (BCECF). NHE activity was assessed by the steady pHi value in the absence of bicarbonate (HEPES). NHE blockade caused a regression of CH similar to that caused by E or N despite the modest decrease in AP. Whereas E and N caused a decrease in NHE activity that persisted after pm isolation, HOE 642 did not. Our data are showing by the first time a regression of CH induced by the blockade of the NHE-1. The increase in steady pHi value in HEPES after chronic treatment with HOE 642 suggests an up-regulation of NHE activity and/or the number of units induced by the chronic blockade.

 

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2nd Virtual Congress of Cardiology

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