Investigations into the mechanisms controlling parturition in cattle.

A pronounced increase in fetal cortisol concentrations stimulating an increase in estrogen production at the expense of progesterone precursors in the placenta, luteolysis, and progesterone withdrawal is considered as a key event during the complex signal cascade leading to the initiation of parturition in cattle. However, there are many questions concerning the exact functional and/or temporal relationships between these individual processes which finally result in the expulsion of the calf and the timely release of the placenta. Thus, parturition was induced in 270-day pregnant cows using the progesterone receptor blocker aglepristone (group AG, n=3), the prostaglandin F(2α) analog cloprostenol (group PG, n=4), and the glucocorticoid dexamethasone (group GC, n=4) to characterize the effect on maternal steroid and prostaglandin levels and to identify immediate subsequent changes in placental morphology and gene expression as compared with untreated controls sampled on day 272 (group D272, n=3) and cows during normal parturition (group NT, n=4). All calves of the treatment groups were born on days 271-272, whereas gestational length in NT cows was 280.5±1.3 days. However, none of the treatments significantly induced the prepartal remodeling of placentomes characterized by a decline in trophoblast giant cells and reduction of the caruncular epithelium. Data on placental CYP17 and COX2 expression confirm that these key enzymes are upregulated by GC, whereas placental aromatase expression was not affected by any treatment. Maternal progesterone and prostaglandin profiles suggest differential effects of the treatments on luteal function and placental or uterine prostaglandin production. The results provide new information on the initiation of parturition in cattle but raise many new questions.