This study was conducted to determine if the chronic failure of weaned sows to return to ovarian cyclicity is due to a decreased capacity of estradiol-17β (E2) to evoke luteinizing hormone (LH) discharge. Primiparous, ovariectomized sows were randomly assigned at five sows/group in a 2 × 4 factorial design. Sows were treated intramuscularly (i.m.) with 0, 2.5, 5.0, or 10.0 μg estradiol-17β benzoate (EB)/kg body weight (BW). Factor A was reproductive state (anestrous or diestrous), and factor B was EB dose. Blood samples were collected prior to EB injection and at 4-h intervals for 7 days after treatment. LH and E2 concentrations were determined by radioimmunoassay (RIA). There was an EB dose effect on the numbers of sows responding to EB with LH surges. Five anestrous and four diestrous sows had LH surges in response to 10 μg EB/kg, whereas 5.0 μg EB/kg induced LH surges in four anestrous and two diestrous sows. One anestrous and none of the diestrous sows had an LH surge when injected with 2.5 μg EB/kg BW. There were no differences in the characteristics of LH surges between ovariectomized anestrous sows and ovariectomized diestrous sows. Mean peak E2 concentration and area under the curve (AUC) were similar between anestrous and diestrous sows, but differed (P < 0.05) between dose of EB. Four ovariectomized, anestrous sows and six ovariectomized, cyclic sows were treated in a second experiment with subcutaneous (s.c.) E2 implants to examine the influence of chronic E2 treatment on LH concentrations. All sows responded to E2 treatment with LH surges. The characteristics of LH release and E2 concentrations were similar between anestrous and cyclic sows. Seemingly, anestrus following weaning does not involve an altered sensitivity of the hypothalamo-hypophyseal axis to the positive feedback effects of E2. © 1990.