Effect of Angiotensin-Converting Enzyme Inhibition and of Angiotension II Receptor Blockade on the Development of Cardiac Hypertrophy in Rats

Comparison of the results of three experimental models of cardiac hypertrophy in rats reveals that angiotensin-converting enzyme (ACE) inhibition and angiotensin (Ang) II receptor blockade have different effects. In the model of pressure-induced left ventricular (LV) overload induced by constriction of the aortic arch, ACE inhibition with ramipril had no effect whatsoever on the development of cardiac hypertrophy both at the gross and the cellular morphological level. This may be because in this particular model, ACE inhibition was prevented from having an effect on blood pressure since the site of aortic constriction was quite near to the left ventricle. It may therefore be hypothezised that the clinical effects of this treatment may be related to the blood pressure-lowering effect. The local renin-angiotensin system (RAS) seems not to play a major role in this experimental model for the hypertrophy process. This is somewhat different in the model of right ventricular (RV) pressure overload induced by pulmonary artery stenosis. The development of RV hypertrophy was not influenced by treatment with ramipril; however, the cell morphology revealed a reduction in cell volume and cross-sectional area. Thus, the typical morphological feature of concentric hypertrophy was attenuated.