Effect of prostacyclin inhibition by tranylcypromine on uterine 6-keto-pgf 1 alpha levels during estrogen hyperemia in rats.
A role for prostacyclin (PGI2) as a mediator of estrogen-induced increases in uterine blood volume (UBV) was investigated by measuring uterine tissue levels of 6-keto-prostaglandin F1 alpha (6-keto-PGF 1 alpha), and testing estrogen responses in rats pretreated with the PGI2 synthesis inhibitor, tranylcypromine (TCP). Uterine 6-keto-PGF1 alpha content was determined by radioimmunoassay of tissue extracts purified through the use of high-performance liquid chromatography (HPLC). Estrogen treatment of castrate rats resulted in a significant increase of uterine 6-keto-PGF 1 alpha was compared to saline treated controls (9.3 ng/uterine horn vs 6.7 ng/uterine horn, p=0.01). Pretreatment with TCP (20 mg/kg) markedly reduced the uterine content of 6-keto-PGF 1 alpha (2.5 ng/uterine horn). The typical 50% increase in UBV observed after estrogen was unaffected by tranylcypromine pretreatment. It was concluded that the increased PGI2 synthesis, as indicated by elevated levels of 6-keto-PGF1 alpha, may function as an amplifying mechanism for the uterine vasodilation-induced by estrogen in castrate rats, but that production of this prostanoid is not essential for the estrogen response.
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism*; D000818:Animals; D011464:Epoprostenol / Q000037:antagonists & inhibitors*; D004967:Estrogens; D005260:Female; D006940:Hyperemia / Q000139:chemically induced*; D011448:Prostaglandin Antagonists; D011817:Rabbits; D011863:Radioimmunoassay; D051381:Rats; D011919:Rats, Inbred Strains; D014191:Tranylcypromine / Q000494:pharmacology*; D014599:Uterus / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism*
D004967:Estrogens; D011448:Prostaglandin Antagonists; D014191:Tranylcypromine; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol