A nongenomic action of estradiol as the suppression of secretion of luteinizing mechanism underlying the acute hormone in ovariectomized ewes

The objective of the present study was to determine how rapidly estradiol (E-2) was able to suppress the secretion of LH in ovariectomized (OVX) ewes and to evaluate the ability of conjugated forms of E-2 (E-2 conjugated to BSA [1,3,5(10)estratrien-3,1 7 beta-diol-6-one-6-carboxymethyloxime-BSA [E BSA] and a novel conjugate, E. conjugated to a small peptide [E-2-PEP]) to mimic the actions of E-2 on secretion of LH and FSH. Animals (n = 5-6 per group) were given infusions for 4 h of 50 mu g of E-2 or equimolar concentrations of E-2-BSA or E-2-PEP. Treatments with E-2, E-2-BSA, and E-2-PEP each induced an acute suppression of LH secretion (<20 min, P < 0.01). In contrast, E-2, but not E-2-BSA or E-2-PEP, induced the characteristic preovulatory-like surge of LH (at 10 h after priming treatment) and decreased secretion of FSH (at 4 h after priming treatment). In conclusion, the acute inhibition of LH secretion induced by E-2 in OVX ewes supports the concept of a nongenomic action as the mechanism underlying the sudden suppression in secretion of LH. In addition, the fact that conjugated forms of E-2 mimicked only the acute suppression of secretion of LH, without inducing the putative genomic actions on secretion of LH or FSH (i.e., a preovulatory-like surge), suggests that the acute effect of E-2 may be mediated via the plasma membrane.