Short Loop Feedback Control of the Estrogen-Induced Luteinizing Hormone Surge in Pigs*

Publisher Website
Google Scholar
Abstract
This study examined whether hCG will block the estradiol-induced LH surge in ovariectomized gilts. Twenty post-puberal cross-bred gilts were ovariectomized at 6-7 months of age. Approximately 2 months later, the experiment was conducted, and all gilts were given estradiol benzoate (EB; 10 .mu.b/kg, im) at 0 h. Controls (n = 6) received 2000 IU hCG im, at 24 h (hCG24; n = 5) or 48 h (hCG48; n = 5) after EB. The fourth group (n = 4) received hCG at 48 h and was then given iv a LHRH agonist (des-Gly10, [D-Ala6]LHRH ethylamide) in 100-ng boluses hourly from 54-96 h after EB. Blood samples for determination of LH and FSH were collected every 6 h from 0-96 h. In controls, EB alone suppressed LH from 3.9 .+-. 1.9 ng/ml at 0 h to 1.0 .+-. 0.2 during 6-48 h (negative feedback), but LH then increased to 4.5 .+-. 0.5 between 54 and 96 h (positive feedback), with the peak of the surge (6.7 .+-. 1.6) occurring at 72 h. Treatment with hCG did not alter LH during the negative feedback phase (1.1 .+-. 0.1 and 1.0 .+-. 0.1 for hCG24 and hCG48, respectively). However, there was no LH surge in gilts given hCG at 24 or 48 h (2.4 .+-. 0.2 and 2.2 .+-. 0.1 from 54-96 h; P < 0.05). Hourly injections of the LHRH agonist evoked a surge in LH (8.3 .+-. 1.3) and maintained elevated LH (4.5 .+-. 0.6) between 54 and 96 h, similar (P > 0.05) to values for controls. Generally, FSH in gilts given hCG followed the same pattern as LH secretion during the negative feedback stage; however, due to randomization, means for the period from 0-48 h for gilts treated with hCG 24 or 48 h after EB were lower (P < 0.05) than for controls or gilts given LHRH agonist (62.2 .+-. 2.8 and 63.0 .+-. 2.7 vs. 79.3 .+-. 3.2 and 93.3 .+-. 4.2 ng/ml, respectively). During the positive feedback phase (54-96 h), FSH was lower in gilts given hCG (hCG24, 63.4 .+-. 2.3; hCG48, 67.3 .+-. 2.0) than in controls (86.0 .+-. 4.0), but in gilts given LHRH agonist, FSH was higher (100.1 .+-. 7.7) than in controls. The treatment by time interaction for FSH in control gilts and gilts given LHRH agonist was significant (P < 0.001) during the positive feedback phase, because FSH surged in gilts given the agonist, but there was no surge in controls. These results demonstrate that hCG prevented the EB-induced surge of LH. We conclude that hCG acts at the hypothalamus or higher brain centers to inhibit LHRH release because the anterior pituitary of hCG-treated gilts release LH in response to hourly doses of a LHRH agonist.