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The presence of pituitary adenylate cyclase-activating peptide (PACAP) 38-immuno-like material (PACAP 38-IL) in the brain and ovary of the crested newt, Triturus carnifex, and its action on ovarian steroidogenesis and prostaglandin synthesis were evaluated. The HPLC, brain and ovary extract peaks that eluted like PACAP 38 were considered PACAP 38-like material. The concentrations of PACAP 38-II in the HPLC extracts were measured by RIA. T. carnifex ovary was incubated with PACAP 38, brain and ovary PACAP 38-IL, and inhibitors of cyclooxygenase (COX), adenylate cyclase (AC) and phospholipase C (PLC) for 30 and 60 min. PACAI 38, and brain and ovary PACAP 38-IL increased prostaglandin E2 (PGE2) (30 and 60 min), and progesterone and corticosterone (60 min), but decreased oestradiol-17 beta (60 min). COX and PLC inhibitors counteracted the increases in PGE2, progesterone and corticosterone and the decrease in oestradiol-17 beta, and the AC, inhibitor also counteracted them except for PGE2. These results suggest that PACAP 38-IL, present in T. carnifex brain and ovary, acts on PLC, inducing the increase of PGE2 which, in turn, acting on AC, induces increases in progesterone and corticosterone and a decrease in oestradiol-17 beta.

Our aim was to study the role of angiotensin-converting enzyme (ACE) and angiotensin II (ANG II) on ovarian steroidogenesis and prostaglandin production of amphibian. Hormonal effects of ACE, ACE inhibitors, synthetic bullfrog angiotensin I (ANG I), and [Val5]ANG II were compared on frog ovaries of postreproductive and prereproductive periods. Very high ACE activity was found in ovary of water frog ( Rana esculenta) compared with other frog tissues, and this activity was inhibited by the typical ACE inhibitors, captopril and lisinopril. Frog ovary tissue in postreproductive and prereproductive periods was incubated in vitro in the presence of ACE (2.5 mU/ml), captopril (0.1 mM), lisinopril (0.1 mM), [Val5]ANG II (1 μM), and synthetic bullfrog ANG I (1 μM). Production of 17β-estradiol, progesterone, androgens, and prostaglandins E2 and F2α was determined. The data showed a modulation of 17β-estradiol, progesterone, and prostaglandin E2 production by ovary ACE; on the other hand, [Val5]ANG II modulated the production of progesterone and prostaglandin F2α, whereas androgen production was not influenced. The present in vitro studies suggest the existence of two pathways independently regulated by ACE and ANG II modulating ovarian steroidogenesis and prostaglandin production.

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