Inhibition by Adrenocorticotrophin of Gonadotrophin-Induced Ovulation in Immature Female Rats

Hagino, Nobuyoshi; Watanabe, Mitsutoshi; Goldzieher, Joseph W.

doi:10.1210/endo-84-2-308

Cited by 88 publications

(50 citation statements)

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“…While the mechanism(s) by which ACTH inhi bits reproductive maturation is not clearly understood, the adrenal glands are essential for this action in rats. ACTH administration does not delay sexual development or block the ovulatory response to PMS in adrenalectomized rats [9,15]. In contrast, ACTH was effective in delaying the onset of puberty in adrenalectomized mice [5].…”

mentioning

confidence: 82%

“…The castrate model was chosen for these studies primarily because the elevated level of LH secretion in these animals made it more feasible to mesure an antigonadotropic action of ACTH. In addition, the inhibitory effect of exogenous ACTH on PMS-induced ovulation in rats is not mediated by the ovaries, but presumably by an inhibitory action of adrenal steroids on gonadotropin secretion [9], Thus in the intact animal, the ACTH-adrenal axis has an inhibitory ef fect on gonadogropin secretion independent of the gonads. With this evidence in mind, we believe our use of the cas trate model to study the mechanism by which ACTH inhi bits sexual maturation is justified.…”

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confidence: 89%

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Influence of Adrenocorticotropin and Adrenalectomy on Gonadotropin Secretion in Immature Rats

1982

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We examined the effects and mechanisms of action of ACTH and ACTH fragments on gonadotropin secretion in immature rats. ACTH administered by daily injection or continuous infusion (osmotic minipumps) attenuated the postcastration rise in serum LH. Pituitary LH concentration was either unchanged or increased in AGTH-treated rats and pituitary sensitivity to gonadotropin-releasing hormone (GnRH) was reduced by ACTH treatment. A fragment of ACTH (ACTH 4-10), which is less steroidogenic, did not alter levels of serum LH, and ACTH did not reduce LH secretion in adrenalectomized castrates. Serum and pituitary concentrations of prolactin were normal in ACTH-treated animals. These studies demonstrate that the suppression of gonadotropin secretion by ACTH is mediated by the adrenal gland. This mechanism causes a decreased pituitary sensitivity to GnRH, but LH synthesis does not appear to be affected. Prolactin does not play a role in this mechanism.

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confidence: 82%

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confidence: 89%

Influence of Adrenocorticotropin and Adrenalectomy on Gonadotropin Secretion in Immature Rats

1982

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“…In early studies, cortisol implants within the medial-basal hypothalamus impaired the de velopment of reproductive organs in prepubertal rats [28], while injections of DEX into the medial preoptic area blocked pregnant mare serum gonadotropin-induced ovu lation in immature females [29]. It was later shown that intracerebroventricular (i.c.v.)…”

Section: Introductionmentioning

confidence: 99%

Antagonism of Type II, but Not Type I Glucocorticoid Receptors Results in Elevated Basal Luteinizing Hormone Release in Male Rats

Briski

Sylvester²

1994

Neuroendocrinology

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The present studies utilized a phaimacologic approach to evaluate the role of corticosterone-preferring mineralocorticoid receptors (type I or MR) versus classic glucocorticoid receptors (type II or GR) in the regulation of basal pituitary luteinizing hormone (LH) secretion in vivo in male rats. Animals bearing indwelling intracardiac venous catheters received a subcutaneous (s.c.) injection of either vehicle, the MR antagonist, RU 752 (0.5 or 5.0 mg/kg body weight), or the GR antagonist, RU 486 (0.5 or 5.0 mg/kg body weight). Additional groups of rats were implanted with indwelling intracerebroventricular (i.c.v.) cannulas and intravenous catheters for drug administration and blood withdrawal, respectively, and injected i.c.v. with vehicle or graded doses (0.1, 1.0 or 10.0 µg/rat) of RU 752 or RU 486. The MR RU 752 failed to alter plasma LH concentrations regardless of dose or route of administration. In contrast, the GR antagonist, RU 486, elicited significant, dose-dependent increases in circulating LH when given either s.c. or i.c.v. Animals injected s.c. with either 0.5 or 5.0 mg RU 486/kg body weight showed elevated plasma LH levels; while the magnitude of this secretory response was not different between the two drug-treated groups, hormone levels remained elevated over baseline for a longer period of time in rats given the higher dose. Central administration of RU 486 at a dose of either 1.0 or 10.0 µg also resulted in elevated LH release; both the magnitude and duration of this increase in plasma LH were dose-dependent. In additional experiments, groups of rats were pretreated with vehicle or the synthetic GR agonist, RU 362, before administration of RU 486. These studies showed that the stimulatory effect of RU 486 on peripheral LH was abolished by prior interaction of GR with the exogenous ligand. In summary, the ability of the GR antagonist, RU 486, to promote an increase in plasma LH concentrations in intact male rats suggests that endogenous glucocorticoids exert a tonic inhibitory tonus on in vivo LH release in these animals, and that GR mediate these suppressive effects. Observations that drug-induced elevations in circulating LH were abolished by pretreatment with the GR agonist, RU 362, suggest that the stimulatory effects of RU 486 on hormone release were achieved by an antiglucocorticoid action. The current findings that plasma LH was increased following intracranial administration of RU 486 implicate central GR in neuroendocrine mechanisms governing pituitary LH.

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“…There can be detrimental effects of heat stress directly on the gametes, the embryo or uterine function, or heat stress may have an indirect effect through alterations of the endocrine system. It has been suggested that heat stress exerts its effect indirectly and that increased glucocorticoids production in a stressed animal blocks or reduces secretion of pituitary gonadotropins [1]. Altered endocrine function in the female could alter gamete and embryo transport, the uterine environment or the conceptus [2].…”

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confidence: 99%

Dietary Administration of Fatty Acids-Enriched Mold Dried Cell Containing .GAMMA.-Linolenic Acid to Female Pigs Improves Ovulation Rate and Embryo Quality in Summer.

Kojima¹,

Zeniya²,

Aoyama

et al. 1997

Journal of Reproduction and Development

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Abstract. The effect of dietary administration with essential unsaturated fatty acids, linoleic acid [18:2 (n-6)], a mixture of oleic acid [18:1 (n-9)], linoleic acid and γ-linolenic acid [18:3 (n-6)], or α-linolenic acid [18:3 (n-3)], on early embryo development of pubertal female pigs in summer was examined. Safflower oil was supplemented to a concentrated diet (the control diet) at the rate of 5% (Safflower oil-diet). The concentration of linoleic acid was 3.75 g/100 g in the Safflower oil-diet. Fatty acids-enriched mold dried cell was supplemented to the control diet at the rate of 20% (Mold dried cell-diet). The concentration of γ-linolenic acid was 5.32 g/100 g in the Mold dried cell-diet. Mold dried cell also contains oleic acid and linoleic acid at concentrations of 7.28 g/100 g and 2.98 g/100 g, respectively. Perilla oil was supplemented to the control diet at the rate of 7.5% (Perilla oil-diet). The concentration of α-linolenic acid was 4.125 g/100 g in the Perilla oil-diet. Each diet was given daily to five crossbred pubertal gilts for approximately 4 months. From at least 70 days after the start of the experimental diets, embryo collections were performed. The control embryos were obtained from the same breed, 10 pubertal gilts, given only the control diet. Embryos were collected on day 6 (day 1=the last day of estrus) and assessed morphologically. Embryo collection was repeated twice for each pig fed the diet supplemented with essential unsaturated fatty acids. The mean number of corpora lutea was greater in gilts given Mold dried cell-diet than in gilts given Safflower oil-diet (P<0.05) or Perilla oil-diet (P<0.01). The mean number of ova recovered in gilts given Mold dried cell-diet was also greater than that in gilts given the control diet (P<0.05), Safflower oil-diet (P<0.05) or Perilla oil-diet (P<0.01). Furthermore, both the mean number and the proportion of embryos showing normal morphology in gilts given Mold dried cell-diet were significantly higher than in gilts given the control diet, Safflower oil-diet or Perilla oil-diet. These results indicate that the unsaturated fatty acids-enriched mold dried cell may be beneficial for improving ovulation rate and embryo quality.

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Inhibition by Adrenocorticotrophin of Gonadotrophin-Induced Ovulation in Immature Female Rats

Cited by 88 publications

References 1 publication

Influence of Adrenocorticotropin and Adrenalectomy on Gonadotropin Secretion in Immature Rats

Influence of Adrenocorticotropin and Adrenalectomy on Gonadotropin Secretion in Immature Rats

Antagonism of Type II, but Not Type I Glucocorticoid Receptors Results in Elevated Basal Luteinizing Hormone Release in Male Rats

Dietary Administration of Fatty Acids-Enriched Mold Dried Cell Containing .GAMMA.-Linolenic Acid to Female Pigs Improves Ovulation Rate and Embryo Quality in Summer.

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