Effects of phosphodiesterase-5 A (PDE5A) inhibition on the hypertrophied myocardium of spontaneously hypertensive rats (SHR).

ESCUDERO DS; DIAZ RG; BREA MS; PORTIANSKY EL; PÉREZ NG

Buenos Aires

Congreso; ISHR XXII World Congress; 2016

International Society of Heart Research

In a previous study we showed that an increased protein Kinase G (PKG) activity after PDE5A inhibition (sildenafil, ?SIL?) inhibits the myocardial Na+/H+ exchanger (NHE1). Since NHE1 hyperactivity is linked to the development of cardiac hypertrophy, our study was aimed to study the potential antihypertrophic effects of SIL on the hypertrophic myocardium of SHR. We initially tested the inhibitory capability of SIL (1μM) on NHE1 in isolated cardiomyocytes of SHR by comparing H+ efflux (JH+) in the absence or presence of SIL at a common pHi of ~6.8, during the pHi recovery from an acidic load (ammonium prepulse in the absence of bicarbonate where the NHE1 is the only active pHi regulatory mechanism). SIL significantly decreased JH+: (mmol /L/ min) 12.93±3.80, n= 5vs. 2.09±0.87, n=4 (P