SARALASIN-INDUCED INHIBITION OF OVULATION IN THE IN-VITRO PERFUSED RAT OVARY IS NOT REPLICATED BY THE ANGIOTENSIN-II TYPE-2 RECEPTOR ANTAGONIST PD123319

OBJECTIVE: Our aim was to explain the effect of the nonspecific angiot ensin II antagonist saralasin and the specific angiotensin II type-2 r eceptor antagonist PD123319 on ovulation. STUDY DESIGN: Saralasin, 1 m u mol/L (n = 5), and PD123319 10 mu mol/L (n = 6), were administered t o in vitro perfused rat ovary. Prostaglandin (prostaglandin E-2, prost aglandin F-2 alpha, 6-keto-prostaglandin F-1 alpha), hydroxy-eicosatet raenoic acid (12-hydroxy-eicosatetraenoic acid, 15-hydroxy-eicosatetra enoic acid), estradiol, and progesterone levels in the perfusate and t he ovulation rate were compared (Mann-Whitney U test) with controls. R ESULTS: Saralasin significantly (P < .01) inhibited the ovulation rate (3.0 +/- 1.4) versus control (13.1 +/- 1.0) and reduced prostaglandin E-2 (at 3 hours P < .01 and 20 hours P < .05) and 6-keto-prostaglandi n F-1 alpha (at 20 hours P < .05) levels. Saralasin did not alter pros taglandin F-2 alpha, hydroxy-eicosatetraenoic acids, or steroid levels . PD123319 decreased 15-hydroxy-eicosatetraenoic acid levels at 3 hour s (P < .05) but had no effects on other eicosanoids, steroid levels, o r the ovulation rate. CONCLUSION: Angiotensin II plays an important ro le in ovulation in the rat and is associated with ovarian prostaglandi n synthesis. This effect is not selectively regulated via the angioten sin II type-2 receptor.