Prostaglandins and follicular functions

Ovulation The involvement of prostaglandins (PGs) in the regulation of ovarian follicular function was first postulated on the basis of the demonstration that inhibitors of prostaglandin synthesis, such as aspirin and indomethacin, were capable of blocking ovulation in rats (Armstrong & Grinwich, 1972; Orczyk & Behrman, 1972). These initial findings were soon confirmed in several other species, including mice (Lau, Saksena & Chang, 1974), rabbits, (Grinwich, Kennedy & Armstrong, 1972; O'Grady, Caldwell, Auletta & Speroff, 1972), rhesus and marmoset monkeys (Wallach, de la Cruz, Hunt, Wright & Stevens, 1975; Maia, Barbosa & Coutinho, 1978), pigs (Ainsworth et al., 1979) and goldfish (Stacey & Pandey, 1975). In two of these species (rabbits and goldfish), the inhibitor was effective when applied locally to the follicle, indicating that the blockade was exerted directly upon the follicle, rather than being mediated via some indirect mechanism, such as through inhibition of gonadotrophin secretion. Further evidence of a role of prostaglandins at the follicular level was provided by the findings that intrafollicular levels of prostaglandins of both the E and F series increased markedly in several of these species shortly before ovulation (Yang, Marsh & LeMaire, 1974; Armstrong, Moon & Zamecnik, 1974; Bauminger & Lindner, 1975; Ainsworth, Baker & Armstrong, 1975; Tsang, Ainsworth, Downey & Armstrong, 1979a); indomethacin, at dosages which prevented ovulation, effectively prevented these increases. The observation that injection of antiserum against PGs blocked the LH-induced ovulation in oestrous rabbits, whether administered systemically (Lau et al., 1974) or via intrafollicular injection (Armstrong et al., 1974), added support to the concept of a role of prostaglandins in ovulation. Antiserum to PGF-2α appeared to be more effective than that to PGE in these experiments, suggesting that PGF-2α was the prostaglandin of greater importance in ovulation.