R S Morris1, I L Wong, R J Paulson. 1. Division of Reproductive Endocrinology, University of Southern California School of Medicine, Los Angeles County Women's and Children's Hospital, USA.
Abstract
PURPOSE: Our purpose was to determine whether angiotensin converting enzyme (ACE) inhibitors affect gonadotropin-stimulated estradiol (E2) production. DESIGN: This was a prospective, masked, randomized, placebo-controlled animal trial. Twenty female New Zealand White rabbits were hyperstimulated with gonadotropins. One-half of the rabbits received concomitant treatment with the ACE inhibitor, enalapril; one-half received concomitant treatment with a placebo. RESULTS: Baseline peripheral E2 (13 +/- 4 vs 11 +/- 2 pg/ml) and angiotensin II (Ang II) (22 +/- 5 vs 27 +/- 7 pg/ml) levels were similar in both groups. Significant inhibition of peripheral Ang II levels was achieved in the enalapril group (32 +/- 6 vs 93 +/- 15 pg/ml; P = 0.005). E2 was significantly higher in the rabbits receiving enalapril versus placebo (369 +/- 58 vs 183 +/- 35 pg/ml, P < 0.03), respectively. By day 10, peripheral E2 had returned to normal levels in both groups (13 +/- 1 vs 13 +/- 1 pg/ml). However, E2 levels in the ovarian effluent were 2.8 times higher in the enalapril rabbits. CONCLUSION: Peripheral Ang II levels increase after gonadotropin stimulation and ACE inhibitors are able to blunt this increase significantly. ACE inhibition has a significant stimulatory effect on ovarian E2 production. This implies that Ang II may normally inhibit ovarian E2 production in stimulated cycles.
PURPOSE: Our purpose was to determine whether angiotensin converting enzyme (ACE) inhibitors affect gonadotropin-stimulated estradiol (E2) production. DESIGN: This was a prospective, masked, randomized, placebo-controlled animal trial. Twenty female New Zealand White rabbits were hyperstimulated with gonadotropins. One-half of the rabbits received concomitant treatment with the ACE inhibitor, enalapril; one-half received concomitant treatment with a placebo. RESULTS: Baseline peripheral E2 (13 +/- 4 vs 11 +/- 2 pg/ml) and angiotensin II (Ang II) (22 +/- 5 vs 27 +/- 7 pg/ml) levels were similar in both groups. Significant inhibition of peripheral Ang II levels was achieved in the enalapril group (32 +/- 6 vs 93 +/- 15 pg/ml; P = 0.005). E2 was significantly higher in the rabbits receiving enalapril versus placebo (369 +/- 58 vs 183 +/- 35 pg/ml, P < 0.03), respectively. By day 10, peripheral E2 had returned to normal levels in both groups (13 +/- 1 vs 13 +/- 1 pg/ml). However, E2 levels in the ovarian effluent were 2.8 times higher in the enalaprilrabbits. CONCLUSION: Peripheral Ang II levels increase after gonadotropin stimulation and ACE inhibitors are able to blunt this increase significantly. ACE inhibition has a significant stimulatory effect on ovarian E2 production. This implies that Ang II may normally inhibit ovarian E2 production in stimulated cycles.