Influence of Ramipril on Right Ventricular Hypertrophy Induced by Pulmonary Artery Stenosis in Rats

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Abstract
The influence of the angiotensin-converting enzyme (ACE) inhibitor ramipril (1 mg/kg orally in a single daily dose on right ventricular (RV) hypertrophy was studied in Sprague Dawley rats. The pulmonary artery was banded to an outer diameter of 1.7 mm. After 14 days, left (LV) and RV hemodynamic parameters were measured in anesthetized animals. Furthermore, regional heart weights were determined, and myocytes of three different heart regions were isolated and subjected to morphometric analysis. Pulmonary artery stenosis caused a marked increase in RV systolic blood pressure (SBP) without alteration of LV functional parameters as compared with sham-operated animals. Correspondingly, the weight of the RV free wall as well as the RV cell volume were increased to about the same extent, while the LV weight was unchanged. Administration of ramipril to pulmonary artery-constricted animals slightly reduced LV SBP and LVdP/dtmax as compared with banded animals without treatment, The increase in RV SBP and the weight gain of the RV free wall were not affected, however. In contrast, the increase in cell volume of isolated myocytes was less pronounced in this group (+27% as compared with +58% in untreated animals). Because there were no differences in water content of the tissue, interstitial or cellular edema cannot be responsible for this discrepancy. Thus, ACE inhibition with ramipril appears to blunt the cellular hypertrophy in this model without affecting the weight gain of the RV.