Investigations into the mechanisms controlling prostaglandin production by the guinea-pig placenta: roles of calcium and gonadotrophin-releasing hormone

The outputs of PGF2 α, PGE2 and 6-keto-PGF1α were higher from the day 29 guinea-pig placenta than from the sub-placenta in culture, with PGF2αbeing the major prostaglandin produced by the placenta. Lack of extracellular calcium reduced the production of all three prostaglandins by the sub-placenta and 6-keto-PGF1 α production by the placenta, but had no effect on the production of PGF2 α and PGE2 by the placenta. EGTA (a calcium chelator) and a low concentration (30 μM) of TMB-8 (an intracellular calcium antagonist) generally inhibited prostaglandin output from the placenta and sub-placenta at various time points during culture, although EGTA had no effect on PGE2 output from the placenta. Trifluoperazine and W-7 (calmodulin inhibitors) had no inhibitory effect on the outputs of PGF2α and PGE2 from the placenta, nor on the outputs of any prostaglandin from the sub-placenta. However, these two compounds inhibited the output of 6-keto-PGF1 α from the placenta. Nifedipine and verapamil (calcium channel blocking drugs) generally reduced the outputs of prostaglandins from the placenta and sub-placenta, except verapamil had no inhibitory effect on PGF2 α output from the sub-placenta. Gonadotrophin-releasing hormone (GnRH) did not stimulate the output of prostaglandins from the placenta, and tended to have a weak inhibitory action on this tissue. On the sub-placenta, GnRH had an initial inhibitory action on the outputs of PGF2α and 6-keto-PGF1 α, which was then followed by a stimulation of the outputs of PGF2α and, to a lesser extent, of PGE2.