Effects of ACE inhibition during fetal development on cardiac microvasculature in adult spontaneously hypertensive rats

Background: Early angiotensin-converting enzyme (ACE) inhibition is able to re-program spontaneously hypertensive rats (SHR) to express an attenuated form of disease in adulthood. Methods: Three groups of animals (n=5 each) were studied: Wistar male rats, SHR males, and SHR males obtained from dams treated with enalapril maleate (15 mg/kg/day) during gestation. Animals were sacrificed 180 days after birth, and hearts were removed for stereological quantification. Volume [Vv] (myocytes, cardiac interstitium and intramyocardial vessels), length [Lv] (intramyocardial vessels), surface [Sv] densities (myocyte and intramyocardial vessels), and the mean cross-sectional area [ā] (myocyte) were estimated. Results: Blood pressure (BP) was lower in Wistar group, higher in SHR group, and intermediate in SHR–enalapril group (respectively: 122±8.4, 194±11.4, and 158±7.6 mm Hg, p<0.0001). Increased Vv (p=0.016), Lv (p<0.01), and Sv (p<0.01) of intramyocardial vessels were observed in SHR–enalapril group when compared to untreated SHR. A small but significant reduction was observed in ā of myocytes (p=0.045). Conclusion: Prenatal ACE inhibition resulted in partial hypertension attenuation as well as left ventricular hypertrophy (LVH). The positive impact on the vascular compartment came along with little or no difference in myocytes and interstitium, suggesting the involvement of a direct mechanism.