The Effect of Adrenocorticotropin or Hydrocortisone on Serum Luteinizing Hormone Concentrations after Adrenalectomy and/or Ovariectomy in the Prepuberal Gilt*

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Abstract
The possible role of ACTH and the adrenal gland in modulating LH [luteinizing hormone] secretion in prepuberal gilts was studied. Fifty-one gilts, 170-175 days of age, were randomly assigned to 12 treatments in a 2 .times. 2 .times. 3 factorial design. The main treatments were adrenalectomy (ADX) or sham-ADX, ovariectomy (OVX) or sham-OVX and ACTH, hydrocortisone acetate (HCA) or vehicle (V) administration. ACTH, HCA or V was administered from days 3-10 after surgery. Beginning at 0800 h on day 10, blood samples were collected every 15 min for 16 h via jugular cannulae. At 1600 and 2000 h, all gilts were injected i.v. with a pharmacological dosage of 400 .mu.g GnRH. ADX and OVX did not influence subsequent serum cortisol (CS) concentrations, detected by RIA [radioimmunoassay]. HCA elevated serum CS concentrations in all 4 surgical groups. ACTH treatment elevated serum CS and progesterone concentrations only in the sham-ADX groups. Every 3 days after surgery, all ADX gilts received 10 mg deoxycorticosterone acetate, i.m., as an electrolyte maintenance treatment, which may have been detected in the peripheral blood by the CS assay since the cross-reaction of deoxycorticosterone with the first antibody of the CS assay was 17.1%. Serum LH concentration, peak frequency and peak magnitude were greater in V-treated OVX gilts than in V-treated sham-OVX gilts in both ADX and sham-ADX groups. Chronic ACTH treatment blocked the increase in basal serum LH concentration, peak frequency and peak magnitude after OVX only when the adrenal glands were present. In contrast, HCA blocked the postcastration increase in the basal serum LH concentration and peak magnitude in the presence or absence of the adrenal glands. However, HCA had no effect on the increased frequency of LH peaks that occurred after OVX in V-treated gilts. The serum LH responses after both GnRH [gonadotropin-releasing hormone] challenges were similar for all gilts, and the LH response to the 2nd GnRH challenge was less than that observed after the 1st challenge. ACTH and HCA suppressed the postcastration increase in LH secretion. However, the effect of ACTH was mediated through the adrenal gland, and the inhibiting influence of ACTH and HCA on LH secretion was apparently not mediated at the pituitary level in the prepuberal gilt.