The present study was undertaken to investigate the effects of prolact
in (PRL) on gonadotropin-induced ovulation and the biosynthesis of pro
staglandin (PG), leukotriene (LT), and plasmin in in vitro perfused ra
bbit ovaries. The addition of PRL to the perfusate inhibited hCG-induc
ed ovulation in vitro in a dose-dependent manner. Although exposure to
hCG significantly increased PGF(2 alpha), PGE(2), and LTB(4) producti
on by perfused rabbit ovaries, PRL did not affect the secretion rates
of PGs and LTB(4) stimulated by hCG administration. The ovarian plasmi
n generation was determined by measuring the amount of plasmin bound t
o its major inhibitor, alpha(2)-plasmin inhibitor (alpha(2)PI-Plm). Ex
posure to hCG enhanced biphasically the ovarian secretion rate of alph
a(2)PI-Plm, while PRL at a dose of 10(3) ng/ml significantly inhibited
the hCG-stimulated generation of alpha(2)PI-Plm in ovaries throughout
the entire perfusion period. A significant correlation was observed b
etween ovulatory efficiency and ovarian plasmin generation in the PRL-
treated ovaries. Additionally, PRL inhibited intrafollicular concentra
tions of alpha(2)PI-Plm in hCG-treated ovaries in a dose-dependent man
ner. These observations substantiate an essential role for a plasmin-g
enerating system in the cascade of events leading to ovulation. In con
clusion, PRL may act directly on the ovary and block ovulation, at lea
st in part, via the inhibition of ovarian plasmin generation.