Prostaglandin D evokes potent uterine contraction via the F prostanoid receptor in postpartum rats.

Prostaglandin (PG) D, a prostanoid known to have hypotensive effect, can evoke increased in vitro prepartum myometrial contraction resulting from up-regulation of the F prostanoid (FP) receptor. The present study further determined postpartum rat uterine responses to PGD to evaluate the possibility of the prostanoid becoming a therapeutic for postpartum uterine atony, a major cause of postpartum hemorrhage that can lead to maternal morbidity. In vitro and in vivo postpartum uterine responses to PGD were determined and compared to those of prepartum rats. Here we show that in postpartum myometrial strips PGD did evoke a contraction sensitive to FP receptor antagonism. Interestingly, this response was not only to a greater extent than that of prepartum rats, but also comparable with the contraction obtained with PGF, a therapeutic for postpartum uterine atony but contradicted in conditions including hypertension. Indeed, PGD was also found to cause increases of basal uterine contraction under in vivo conditions. Western blots revealed that the expression of FP receptors in postpartum myometrium was higher than that of prepartum rats. Moreover, we noted that the amount of PGD produced in postpartum uteri, although lower than that of prepartum rats, was increased compared to non-pregnant conditions. These results thus demonstrate that due to a further up-regulation or high expression of myometrial FP receptors, PGD can evoke potent uterine contraction postpartum, and hence the prostanoid, which is naturally synthesized in uterine tissues, could be a potential therapeutic for postpartum uterine atony, especially in settings, such as hypertension.