\ m=-\ 1 (decrease to 33 \ m=+-\7% and 31 \ m=+-\ 5% of control culture values, respectively). Addition of LH to the media increased inhibitor activity 3.04 \ m=+-\ 0.39 times compared with the control; however, A23187 (10 and 100 \g=m\mol l\m=-\1 ), in the presence of LH, decreased inhibitor activity by approximately 67%. The ionophore had disparate effects on progesterone production. Without LH, A23187 increased progesterone production by 2.96 \ m=+-\ 0.47 times at 10 \g=m\mol l\m=-\1and by 5.53 \ m=+-\ 0.65 times at 100 \g=m\mol l \ m=-\ 1 . However, in LH-stimulated cells, progesterone was inhibited by A23187 at 1 and 10 \g=m\mol l\m=-\1but was unchanged at 100 \g=m\mol l \m=-\1. In the angiotensin experiment, addition of AII (0\p=n-\10 000 nmol l\m=-\1 ) or saralasin (1 \g=m\mol l\m=-\1 ) did not affect inhibitor activity or progesterone concentrations compared with control values in the absence or presence of LH. For the angiotensin experiment in vivo, PMSG-primed rats were injected with hCG followed by saralasin (10 mmol l \ m=-\ 1 ) 1 or 3 h later and killed at 4, 8, or 12 h after hCG. Expression of the ovarian tissue inhibitor of metalloproteinase-1 (TIMP-1) increased by 1.7 times at 4 h, 3.3 times at 8 h, and 3.0 times at 12 h after hCG compared with values in ovaries collected at the time of hCG injection. Administration of saralasin at 1 or 3 h after hCG had no effect on expression of TIMP-1 or on serum concentrations of progesterone or oestradiol. In summary, A23187 decreased granulosa cell-derived inhibitor activity, whereas AII had no effect. We propose that calcium may play a role in modulating proteolysis associated with ovulation, while AII does not appear to regulate ovarian metalloproteinase inhibitor activity.
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