Myometria and aortae from non-pregnant and ovariectomized rats when chopped and incubated in Krebs solution (50% and 25% w/v) respectively) at 20° C released an anti-aggregatory material. This substance resembled PGI2 in its properties (being stable at pH 12 and losing anti-aggregatory activity on acidification). It was conclusively identified as by detection of the hydrolytic product 6-oxo PGF using GC/MS. Aortae from the same rats released greater amounts of than the myometrium and the generation of the substance increased steadily with incubation times. Myometrial production of PGI2 peaked after 30 min of incubation. The generation of PGI2 by both myometrium and aorta varied during the oestrous cycle with minimum output seen at oestrous and maximal production at dioestrous. Administration of ovarian hormones (in-vivo or in-vitro) produced different effects on myometrial and aortic PGI2 release. The hormones increased aortic and decreased myometrial PGI2 formation. Aortic PGI2 synthesis also dramatically increased on day 21 of gestation compared to day 20. However, aortae taken from 20-day pregnant rats released a similar amount of PGI2 to those taken from non-pregnant rats (in oestrous) or male rats. The in-vitro stimulant effect of diethylstilboestrol (ST) on aortic PGI2 formation was blocked by mepacrine, protein synthesis inhibitors (cycloheximide and puromycin) and the anti-oestrogen ethamoxy-triphetol. This was also true for the effect of progesterone on aortic PGI2 production. On the other hand, the inhibitory influence of ST on myometrial PGI2 formation was partially reversed by phospholipase A2 and arachidonic acid, but it was resistant to protein synthesis inhibitors and ethamoxytriphetol.
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