Prostaglandin production by the guinea-pig endometrium: is calcium necessary?

Abstract
The output of prostaglandin (PG) F from guinea-pig endometrium obtained on day 15 of the oestrous cycle and maintained in tissue culture was significantly (P2+-depleted medium, EGTA (a Ca2+ chelator), 8-(N,N-diethyl-amino)octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8; an intracellular Ca2+ antagonist), trifluoperazine (TFP) and N-(6-aminohexyl)-5-chloro-1-naphthalenesulphonamide (W-7; both calmodulin antagonists). Nifedipine inhibited PGF output at a concentration (100 μmol/l) much greater than that usually required to block Ca2+ channels. Verapamil had a small but significant (P < 0·05) inhibitory effect on PGF output at 10–100 μmol/l. The outputs of PGE2 and, to a lesser extent, 6-keto-PGF (the hydrated product of PGI2) were also reduced by using Ca2+-depleted medium. EGTA reduced the outputs of PGE2 and 6-keto-PGF on day 1 of culture, but stimulated 6-keto-PGF output on day 3 of culture. The outputs of PGE2 and 6-keto-PGF were increased by TMB-8 (100 μmol/l) on day 3 of culture and by TFP and, to a smaller extent, by W-7 on all 3 days of culture. Nifedipine (100 μmol/l by not 1 or 10 μmol/l) reduced the outputs of PGE2 and 6-keto-PGF on all 3 days of culture, whereas verapamil (100 μmol/l but not 1 or 10 μmol/l) increased the outputs of these two prostaglandins on days 2 and 3 of culture. Phorbol 12-myristate 13-acetate (an activator of protein kinase C) had no effect on the outputs of PGF, PGE2 and 6-keto-PGF from cultured guineapig endometrium obtained on days 7 and 15 of the oestrous cycle. It is concluded that extracellular Ca2+ is necessary for the high output of PGF from the guinea-pig uterus after day 11 of the oestrous cycle, and that the action of Ca2+ is not potentiated by the activation of protein kinase C. J. Endocr. (1987) 113, 463–471