Influence of estradiol and fetal stress on luteinizing hormone, follicle-stimulating hormone, and prolactin in late-gestation fetal sheep.

BACKGROUND Hypotension and reduced cerebral blood flow secondary to brachiocephalic occlusion (BCO) stimulate various homeostatic physiological and endocrine responses. Our previous studies have also suggested a role of estradiol in augmenting the fetal stress response to BCO. OBJECTIVES We tested the hypothesis that gonadotropins and/or prolactin (PRL) are upregulated in fetal pituitary in response to fetal stress and play a role in the response to BCO-induced stress. METHODS We performed 3 studies: one in which we measured ovine fetal pituitary PRL, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) mRNA throughout the latter half of gestation in order to better understand the ontogenetic changes upon which dynamic responses are superimposed; one in which we measured these mRNA abundances in response to BCO and/or estrogen treatment, and one in which we measured plasma LH responses to BCO in chronically catheterized late-gestation fetal sheep. RESULTS PRL gene expression is increased dramatically in the last 20% of gestation. LH and FSH mRNAs were unchanged except for a transient dip in the expression of LH in the last few days before the normal time of spontaneous parturition. Chronic treatment with estradiol decreased LH and FSH mRNA, but increased PRL mRNA abundance after BCO. In contrast, BCO alone increases the abundance of LH, but not FSH or PRL mRNA in fetal pituitary. Plasma LH concentrations were not increased in response to BCO. CONCLUSIONS We conclude that the late-gestation fetal sheep responds to hypotensive stress with increases in LH mRNA but not LH secretion. LH, FSH and PRL changes are therefore unlikely to contribute to the fetal response to cerebral hypoperfusion.