Endocrinology, Vol 126, 3107-3115, Copyright © 1990 by Endocrine Society

ARTICLES

Continuous and pulsatile infusions of luteinizing hormone have identical effects on steroidogenic capacity and sensitivity of Leydig cells in rats passively immunized against gonadotropin-releasing hormone

KL Gibson-Berry and DJ Chase
Department of Biological Sciences, State University of New York, Binghamton 13901.

Adult male rats were passively immunized against GnRH and given iv infusions of saline or 60 or 300 ng NIDDK ovine LH-24/100 g BW.24 h in continuous regimens of 2.5 or 12.5 ng/100 g BW.h and pulsatile regimens of 1-min pulses of 5 or 25 ng/100 g BW every 2 h. Control animals were treated with nonimmune serum and saline. After 10 days of in vivo treatment, Leydig cells were purified and incubated in vitro with 1) increasing concentrations of hCG (0-50 mIU/ml) in the presence or absence of methylisobutylxanthine, 2) a maximally stimulatory concentration of 8-bromo-cAMP (8-Br-cAMP; 1 mM), and 3) a saturating concentration of 25-hydroxycholesterol (10 microM). LH receptor concentrations were quantified by [125I]hCG binding assay. Maximum testosterone production in the presence of hCG, 8-Br-cAMP, or 25- hydroxycholesterol was reduced by more than 90% in Leydig cells from anti-GnRH serum-treated rats (compared to that in cells from control rats), and this reduction in steroidogenic capacity was prevented in a dose-dependent manner by concurrent infusion of LH in either the continuous or pulsatile regimens. These results confirm that the trophic actions of LH on Leydig cells in vivo 1) do not depend on pulsatile secretion of the hormone, and 2) include induction/maintenance of one or more of the enzymes catalyzing the conversion of cholesterol to testosterone. Trophic actions on constituents or processes before cholesterol side-chain cleavage were not apparent; in vivo treatments had no obvious differential effects on hCG-stimulated, 8-Br-cAMP-stimulated, or 25-hydroxycholesterol- supported testosterone production. Sensitivity to hCG was increased (EC50 for stimulation of testosterone production was decreased) by passive immunization against GnRH, and this effect was prevented in a dose-dependent manner by concurrent infusion of LH in either the continuous or pulsatile regimens. Thus, intermittent exposure to low concentrations of LH in vivo desensitizes Leydig cells as effectively as continuous exposure. Neither specific binding of [125I]hCG nor the effect of methylisobutylxanthine on sensitivity to hCG in vitro differed among treatment groups. Therefore, both the trophic and desensitizing actions of LH appear to occur by mechanisms that are independent of changes in available LH receptor concentration and phosphodiesterase activity.

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