Testosterone feedback on FSH secretion in male sheep

D’Occhio, M. J.; Schanbacher, B. D.; Kinder, J. E.

doi:10.1530/jrf.0.0660699

Cited by 14 publications

(6 citation statements)

References 12 publications

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“…This aggregation effect will be less pronounced in the perfused tissue used in the present study as space left after shrinkage of the seminiferous epithelium is partly accounted for by the dilated lymphatics. Kerr, Rich & de Kretser (1979) have confirmed the impressions of earlier workers (Hanes, 1911;Lynch & Scott, 1951) (Chemes, Ri varóla & Bergada, 1976;Christensen & Peacock, 1980 (Schanbacher, 1979a;1980 (Schanbacher, 1979b;D'Occhio, Schanbacher & Kinder, 1982 (Catt et al, 1980) and an LHRH-like factor produced by the seminiferous tubule (Sharpe, Fraser, Cooper & Rommerts, 1981) have been shown to exert an intratesticular control of Leydig cell steroidogenesis, the relationship between these substances and Leydig cell structure and function has not yet been investigated. The role of the seminiferous epithelium in exerting some control of Leydig cell activity has been emphasized by Ucci (1982), who showed that there was an inverse relationship between Leydig cell size and activity, and germ cell maturation in the normal urodele testis.…”

Section: Morphometrysupporting

confidence: 72%

Effect of scrotal insulation on the pituitary--testicular axis of the ram

Byers¹,

Glover²

1984

Reproduction

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Section: Morphometrysupporting

confidence: 72%

Effect of scrotal insulation on the pituitary--testicular axis of the ram

Byers¹,

Glover²

1984

Reproduction

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“…The alternative possibility that infused 5a-dihydrotestosterone altered LH release indirectly by displacing endogenous testosterone from its plasma binding sites is unlikely under these equilibrium conditions, since injected 5a-dihydrotestosterone actually decreases plasma free testosterone concentrations in men within 24-48 h (54). As important, the selectivity of this infusion schedule in suppressing LH pulse frequency without reducing LH pulse amplitude closely mimics the effects of low-dosage (but not pharmacological dosage) androgen replacement in other species, such as the rodent, sheep, and Rhesus monkey (55)(56)(57).…”

Section: Discussionmentioning

confidence: 89%

Role of endogenous opiates in the expression of negative feedback actions of androgen and estrogen on pulsatile properties of luteinizing hormone secretion in man.

Veldhuis¹,

Rogol²,

Samojlik³

et al. 1984

J. Clin. Invest.

193

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As bstract. We have tested the participation of endogenous opiate pathways in the negative feedback actions of gonadal steroids on pulsatile properties of luteinizing (LH) hormone release in normal men. To this end, sex steroid hormones were infused intravenously at dosages that under steady state conditions selectively suppressed either the frequency or the amplitude of the pulsatile LH signal. The properties of pulsatile LH secretion were assessed quantitatively by computerized analysis of LH series derived from serial blood sampling over 12 h of observation.When the pure (nonaromatizable) androgen, 5-a-dihydrotestosterone, was infused continuously for 108 h at the blood production rate of testosterone, we were able to achieve selective inhibition ofLH pulse frequency akin to that observed in experimental animals after low-dosage androgen replacement. Under these conditions, serum concentrations of testosterone and estradiol-1 7,3 did not change significantly, but serum 5a-dihydrotestosterone concentrations increased approximately two-to threefold, with a corresponding increase in levels of its major me- tabolite, 5a-androstan-3a, 17f-diol. In separate experiments, the infusion of estradiol-1 7#3 at its blood production rate over a 4.5-d interval selectively suppressed LH pulse amplitude without influencing LH pulse frequency. Estrogen infusion increased serum estradiol-1 73 levels approximately twofold without significantly altering blood androgen concentrations. We then used these schedules of selective androgen or estrogen infusion to investigate the participation of endogenous opiates in the individual inhibitory feedback actions of pure androgen or estrogen on pulsatile LH release by administering a potent and specific opiate-receptor antagonist, naltrexone, during the infusions.Our observations indicate that, despite the continuous infusion of a dosage of 5a-dihydrotestosterone that significantly suppresses LH pulse frequency, co-administration of an opiate-receptor antagonist effectively reinstates LH pulse frequency to control levels. Moreover, during the infusion of a suppressive dose of estradiol-1 73, opiate receptor blockade significantly augments LH pulse frequency and increases LH peak amplitude to control levels.Thus, the present studies in normal men demonstrate for the first time that the selective inhibitory action of a pure androgen on LH pulse frequency is effectively antagonized by opiate-receptor blockade. This pivotal oW servation indicates that opiatergic and androgen-dependent mechanisms specifically and coordinately control the hypothalamic pulse generator for gonadotropin-re- We conclude that the negative feedback actions of gonadal steroids are integrally coupled to endogenous opiate pathways and that such functional coupling is ultimately expressed at least in part at the level of the hypothalamic pulse generator for GnRH. These observations suggest a model for the proximate regulation of gonadotropin secretion in man, in which the regulatory actions of two major inhibitory systems...

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“…Oestradiol is also a potent inhibitor of FSH as shown by the immunization of rams (Sanford, 1987) and by replacement studies in rams (Sanford & Robaire, 1990), bulls ) and stallions (Thompson et al 1979). The relative importance of testosterone and oestradiol is unclear, as replacement of physiological levels of testosterone to recently castrated rams resulted in FSH concentrations that were within the physiological range (D'Occhio et al 1982), whereas oestradiol is more effective than testosterone alone in long-term castrated animals (D'Occhio, Galil, Brooks & Setchell, 1985), giving rise to the theory that the pituitary gland becomes insensitive to testosterone feedback with time after castration. In the stallion, however, oestradiol was more potent than testoster¬ one in short-term castrated animals, possibly reflecting the high secretion rate of testicular oestrogens in this species (Thompson et al 1979).…”

Section: Malesmentioning

confidence: 99%