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Journal of Animal Science, Vol 68, Issue 4 1077-1086, Copyright © 1990 by American Society of Animal Science

JOURNAL ARTICLE

Estradiol feedback inhibition of luteinizing hormone concentrations in the anestrous sow

G. W. Almond and G. D. Dial
North Carolina State University, Raleigh 27606.

The suppressive effects of exogenous 17 beta-estradiol (E2) on LH concentrations in sows that remained anestrus following weaning and in those that returned to estrus were evaluated. Four anestrous and four cyclic sows were treated subcutaneously with silastic implants containing E2 at 13 d after ovariectomy (d 0). Three anestrous and six cyclic sows received silastic implants without E2. Blood was collected at 6-h intervals from d -1 to d 12 and at 15-min intervals for 8 h on d -1, 2, 7 and 12. Sows were treated with 1 microgram GnRH/kg BW at the completion of each 8-h frequent sampling period. Blood was collected at intervals of 10 to 30 min for 3 h after GnRH treatment. Concentrations of E2 remained less than 5 pg/ml in sham-treated sows and were between 20 and 25 pg/ml in E2-treated females. Pulsatile LH concentrations was similar between anestrous and cyclic sows prior to implant treatment. Sham-treated anestrous sows had greater (P less than .05) pulse frequency and mean LH concentrations than E2-treated anestrous sows on d 2, 7 and 12. Differences in pulsatile LH concentrations between E2-treated and sham-treated cyclic sows were not detected. Pulse frequency was less (P less than .05) in E2-treated anestrous sows than in E2-treated cyclic sows on d 7 and 12. Peak LH concentrations were greater (P less than .05) in E2-treated cyclic sows than in E2-treated anestrous sows at each GnRH challenge. These results suggest that the hypothalamo-hypophyseal axis is more sensitive to the negative feedback effects of E2 in anestrous sows than in cyclic sows. In addition, chronic E2 treatment reduces pituitary responsiveness to GnRH to a greater extent in anestrous than in cyclic sows. Failure to return to estrus in swine may be due, at least in part, to an increased sensitivity of the hypothalamo-hypophyseal axis to the negative feedback effect of estradiol.


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Copyright © 1990 by the American Society of Animal Science.