Luteinizing hormone secretion in hypophysial stalk-transected gilts given hydrocortisone acetate and pulsatile gonadotropin-releasing hormone

Estienne, M. J.; Barb, C. R.; Kesner, James S.; Kraeling, Robert R.; Rampacek, George B.

doi:10.1016/0739-7240(91)90008-8

Cited by 23 publications

(8 citation statements)

References 36 publications

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“…Past studies have provided evidence for inhibitory actions at both the hypothalamic and pituitary levels in the absence of direct in vivo assessment of endogenous GnRH in combination with LH pulsatility (7)(8)(9)(10)(11)(12)(13)27). Here, we determined the impact of a defined elevation in cortisol at both the hypothalamic and pituitary levels.…”

Section: Discussionmentioning

confidence: 94%

“…On the other hand, observations in gonadectomized rhesus monkeys and pigs provide evidence that, when elevated chronically, cortisol acts at the hypothalamic level to inhibit pulsatile GnRH release. In the latter studies, however, the approach was indirect as GnRH suppression was inferred from the lack of a reduction in pituitary responsiveness to GnRH (12,13). Our goal in the present study was to distinguish between hypothalamic and pituitary sites for the acute inhibitory action of cortisol on pulsatile LH secretion in ovariectomized ewes.…”

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confidence: 94%

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Does Cortisol Inhibit Pulsatile Luteinizing Hormone Secretion at the Hypothalamic or Pituitary Level?

2004

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Elevations in glucocorticoids suppress pulsatile LH secretion in sheep, but the neuroendocrine sites and mechanisms of this disruption remain unclear. Here, we conducted two experiments in ovariectomized ewes to determine whether an acute increase in plasma cortisol inhibits pulsatile LH secretion by suppressing GnRH release into pituitary portal blood or by inhibiting pituitary responsiveness to GnRH. First, we sampled pituitary portal and peripheral blood after administration of cortisol to mimic the elevation stimulated by an immune/inflammatory stress. Within 1 h, cortisol inhibited LH pulse amplitude. LH pulse frequency, however, was unaffected. In contrast, cortisol did not suppress either parameter of GnRH secretion. Next, we assessed the effect of cortisol on pituitary responsiveness to exogenous GnRH pulses of fixed amplitude, duration, and frequency. Hourly pulses of GnRH were delivered to ewes in which endogenous GnRH secretion was blocked by estradiol. Cortisol, again, rapidly and robustly suppressed the amplitude of GnRH-induced LH pulses. We conclude that, in the ovariectomized ewe, cortisol suppresses pulsatile LH secretion by inhibiting pituitary responsiveness to GnRH rather than by suppressing hypothalamic GnRH release.

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Section: Discussionmentioning

confidence: 94%

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confidence: 94%

Does Cortisol Inhibit Pulsatile Luteinizing Hormone Secretion at the Hypothalamic or Pituitary Level?

2004

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“…Studies with different models of stress i m i t a t i o n h a v e d e m o n s t r a t e d t h a t b o t h administration of ACTH or cortisol impaired reproductive function in female pigs when given in a way which resulted in a sustained elevation of cortisol in plasma [17][18][19]. Furthermore, cortisol was shown to affect the LH secretion preferentially by reducing the frequency and amplitude of GnRH pulses [20,21], and by effects at pituitary level [22].…”

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confidence: 99%

Alteration of Reproductive Hormone Levels in Pregnant Sows Induced by Repeated ACTH Application and Its Possible Influence on Pre- and Post-natal Hormone Secretion of Piglets

Brüssow¹,

Schneider²,

Kanitz

et al. 2005

Journal of Reproduction and Development

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Abstract. Prenatal stress has been seen as a reason for reproductive failures in pig offspring mostly originated or mediated by changed maternal functions. Experiments were conducted in pregnant gilts (n=32) to characterize effects of elevated maternal glucocorticoids on the secretion of reproductive hormones (LH, progesterone) during the 1 st (EXP 1), 2 nd (EXP 2) and 3 rd (EXP 3) trimester of pregnancy (TP). Transiently elevated cortisol release was repeatedly achieved by application of 100 IU adenocorticotropic hormone (ACTH) (Synacthen Depot®) six times every second day beginning either on day 28 (EXP 1), day 49 (EXP 2) or day 75 of pregnancy (EXP 3). Glucocorticoid concentrations were examined in umbilical blood vessels of fetuses which mothers were subjected to ACTH at 2 nd and 3 rd TP (EXP 4). Furthermore, the pituitary function of newborn piglets of EXP 2 was checked by a LH-RH challenge test. In sows, LH concentrations were at low basal level (0.1-0.2 ng/ ml) but with pulsatory release pattern during each TP. The number of LH pulses/6 h (LSM ± SE) of saline treated Controls increased with ongoing pregnancy and decreased to the 3 rd TP (1.3 ± 0.2 in EXP 1 vs. 2.0 ± 0.1 in EXP 2 vs. 1.4 ± 0.1 in EXP 3, p<0.05). After ACTH treatment the number of LH pulses left unchanged in Experiments 1 and 2 (1.3 ± 0.2 and 1.5 ± 0.1) and decreased in EXP 3 (0.8 ± 0.2, p<0.05). Differences (p<0.05) were obtained comparing the LH pulse number of ACTH and saline treated sows at the 2 nd and 3 rd TP. Moreover, areas under the curve (AUC) of each LH pulse and of LH over baseline were significantly reduced by treatment. Levels of progesterone increased (p<0.05) for 150 to 170 min after each ACTH application both in EXP 1 and EXP 2, but not in EXP 3. The mean progesterone concentration was different between trimesters, and ACTH and Controls (1 st TP: 30.0 ± 0.9 and 24.4 ± 0.7 ng/ml; 2 nd TP: 35.5 ± 0.9 and 29.1 ± 1.0 ng/ml; 3 rd TP: 13.6 ± 0.2 and 13.1 ± 0.1 ng/ml; p<0.05). In fetuses (n=87) recovered 3 h after ACTH or saline (EXP 4), the plasma cortisol concentrations were significantly increased in umbilical vein (93.7 ± 5.5 vs. 47.0 ± 5.3 nmol/l) and artery (95.7 ± 5.4 vs. 66.4 ± 5.4 nmol/l), and in periphery (46.8 ± 5.3 vs. 27.1 ± 5.3 nmol/l) compared to controls. Plasma ACTH concentrations, however, did not differ in fetuses of both treatment groups. Postnatal LH-RH challenge tests (1 st and 28 th day post partum) induced LH surges in female piglets (n=67) both of ACTH and saline treated sows, but did not differ between groups (1 st day: 7.2 ± 0.8 vs. 8.1 ± 0.7 ng/ml; 28 th day: 10.5 ± 1.7 vs. 13.6 ± 2.2 ng/ml). However, basal LH of piglets whose mothers were submitted to ACTH during 2 nd TP was lower on 1 st day (1.7 ± 0.2 vs. 2.3 ± 0.2 ng/ml, p<0.05) but not on 28 th day (1.0 ± 0.2 vs. 1.1 ± 0.2 ng/ml). However in both groups, the basal LH was always higher on 1 st as on 28 th day (p<0.05). Thus, chronic intermittent ACTH administration is able to influence the release pattern of maternal reproductive hormones. However, ...

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“…The effects of elevated glucocorticoids are primarily mediated by GR which are highly expressed in CRH neurons and function in HPA axis regulation (De Kloet et al, 1998), but also in hypothalamic areas critical for GnRH neuron regulation (Dufourny and Skinner, 2002; Takumi et al, 2012), including expression in GnRH neurons in the rat (Ahima and Harlan, 1992). Early seminal studies implicated an action of cortisol at the hypothalamic level to inhibit pulsatile GnRH release by demonstrating in gonadectomized rhesus monkeys and pigs that chronic administration of glucocorticoids suppresses mean LH secretion in the absence of a reduction in pituitary responsiveness to a GnRH challenge (Dubey and Plant, 1985; Estienne et al, 1991). Inhibition at the hypothalamic level is further supported by evidence that glucocorticoids reduce the frequency of LH pulses in ovary-intact female sheep, ovariectomized female rats, and women during the follicular phase of the ovulatory cycle (Breen et al, 2005; Li et al, 2004; Saketos et al, 1993).…”

Section: Neuroendocrine Site Of Glucocorticoid Action During Stressmentioning

confidence: 99%

Influence of stress-induced intermediates on gonadotropin gene expression in gonadotrope cells

Breen

Mellon

2014

Molecular and Cellular Endocrinology

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Despite extensive investigation, a comprehensive understanding of the mechanisms whereby stress impacts fertility remains elusive. Since the 1930s, when Hans Selye popularized studying adaptations to stress (Selye, 1937), we have learned that compensatory mechanisms involve a complex interplay of neural and hormonal processes that allow various body functions to adjust to stress, in a coordinated manner. In terms of reproduction, the adjustment to a stressor interferes with integrated functioning at multiple levels of regulation – the hypothalamus, anterior pituitary gland, gonads, and neural centers coordinating behavior. Various mediators are postulated to participate in reproductive suppression. These include catecholamines, cytokines, prostaglandins, endogenous opioid peptides, and hormones of the hypothalamic-pituitary-adrenal axis. This review focuses on one class of mediators, the glucocorticoids, and provides our views on the relevance and mode of action of this inhibitory intermediate within the anterior pituitary gonadotrope, as a potential cellular site whereby glucocorticoids contribute to stress-induced reproductive suppression.

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Luteinizing hormone secretion in hypophysial stalk-transected gilts given hydrocortisone acetate and pulsatile gonadotropin-releasing hormone

Cited by 23 publications

References 36 publications

Does Cortisol Inhibit Pulsatile Luteinizing Hormone Secretion at the Hypothalamic or Pituitary Level?

Does Cortisol Inhibit Pulsatile Luteinizing Hormone Secretion at the Hypothalamic or Pituitary Level?

Alteration of Reproductive Hormone Levels in Pregnant Sows Induced by Repeated ACTH Application and Its Possible Influence on Pre- and Post-natal Hormone Secretion of Piglets

Influence of stress-induced intermediates on gonadotropin gene expression in gonadotrope cells

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