title: Effects of hydrocortisone, oestradiol and progesterone on A23187-stimulated prostaglandin output from the guinea-pig uterus superfused in vitro.
abstract: Hydrocortisone (10 micrograms/ml) had no effect on the basal outputs and A23187-stimulated outputs of PGF2 alpha, PGE2 and 6-keto-PGF1 alpha from the Day 15 guinea-pig uterus superfused in vitro. These findings indicate that the high output of PGF2 alpha from the guinea-pig uterus during the last one-third of the oestrous cycle is not modulated by the adrenal glucocorticoid hormones. Progesterone (10 micrograms/ml) had no effect on the A23187-induced increases in PG output from the Day 15 guinea-pig uterus. However, oestradiol (10 micrograms/ml but not 1 microgram/ml) significantly reduced the increases in outputs of PGF2 alpha, PGE2 and 6-keto-PGF1 alpha induced by A23187 from the Day 15 guinea-pig uterus, without affecting basal PG outputs. The increase in uterine tone induced by A23187 in the Day 15 guinea-pig uterus was reduced by 20-50% by oestradiol (10 micrograms/ml). The addition of oestradiol (10 micrograms/ml) and progesterone together (10 micrograms/ml) produced the same effects on the Day 15 guinea-pig uterus as oestradiol alone. Oestradiol (10 micrograms/ml) also reduced the A23187-induced increases in PG output from the Day 7 guinea-pig uterus, but did not reduce the increase in uterine tone. Oestradiol (10 micrograms/ml) reduced the increases in outputs of PGF2 alpha, PGE2 and 6-keto-PGF1 alpha induced by exogenous arachidonic acid from the Day 7 and Day 15 guinea-pig uterus. Previous studies have shown that oestradiol is not a cyclo-oxygenase inhibitor. The present findings suggest that oestradiol, at a relatively high concentration, may interfere with the access of arachidonic acid to the cyclo-oxygenase enzyme. This action of oestradiol may explain its anti-luteolytic action when administered to guinea-pigs in large doses after Day 9 of the cycle.
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology*; D015237:Dinoprost; D015232:Dinoprostone; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D006168:Guinea Pigs; D006854:Hydrocortisone / Q000494:pharmacology*; D066298:In Vitro Techniques; D011374:Progesterone / Q000494:pharmacology*; D011453:Prostaglandins / Q000096:biosynthesis* / Q000378:metabolism; D011458:Prostaglandins E / Q000096:biosynthesis; D011460:Prostaglandins F / Q000096:biosynthesis; D013268:Stimulation, Chemical; D014590:Uterine Contraction / Q000187:drug effects; D014599:Uterus / Q000187:drug effects / Q000378:metabolism*
chemical_list: D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D000001:Calcimycin; D011374:Progesterone; D004958:Estradiol; D015121:6-Ketoprostaglandin F1 alpha; D015237:Dinoprost; D015232:Dinoprostone; D006854:Hydrocortisone