A Role for Vasopressin in the Stress‐Induced Inhibition of Gonadotrophin Secretion: Studies in the Brattleboro Rat

Cover, Patricia O.; Laycock, John; Gartside, I B; Buckingham, Julia C.

doi:10.1111/j.1365-2826.1991.tb00296.x

Cited by 9 publications

(9 citation statements)

References 41 publications

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“…Basal A C T H and p -E N D levels were the same in DI and L E rats. For A C T H this is in agreement with some studies [24,26] while other studies have shown lower basal A C T H levels in D I rats when compared to LE rats [27][28][29].…”

Section: Discussionsupporting

confidence: 92%

“…For A C T H , this finding is in agreement with previous studies where the A C T H response to other stressors was found to be smaller in D I than in LE rats [28,29]. Furthermore, some earlier studies showed an im paired corticosterone response to stress [30][31][32][33], but these results do not necessarily reflect the A C T H secre tion since the adrenal response to A C T H may be lower in D I rats [33].…”

Section: Discussionsupporting

confidence: 82%

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Impaired Histamine- and Stress-Induced Secretion of ACTH and β-Endorphin in Vasopressin- Deficient Brattleboro Rats

Kjær¹,

Knigge²,

Bach³

et al. 1993

Neuroendocrinology

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Arginine vasopressin (AVP), corticotropin-releasing hormone (CRH) and catecholamines seem to be involved in the histamine- (HA) and/or stress-induced release of the pro-opiomelanocortin-derived peptides adrenocorticotropic hormone (ACTH) and β-endorphin (β-END). The AVP component of the regulatory mechanism can be specifically studied in Brattleboro rats which lack AVP. These animals may therefore serve as a useful biological model for investigating the importance of AVP in the ACTH and β-END response to HA and stress. On this background, we studied the ACTH and β-END response to HA or restraint stress in conscious, male dizygotic AVP-deficient Brattleboro rats (DI) and compared the hypothalamic content of CRH and catecholamines in these rats with that of nondiabetic isogenic Long-Evans rats (LE). In addition, we studied the hypothalamic AVP content in LE rats after HA infusion or exposure to restraint stress. HA (270 nmol) administered intracerebroventricularly (i.c.v.) or 5 min of restraint stress caused a 6- to 7-fold increase in plasma concentrations of ACTH and β-END in LE rats but only a 2- to 3-fold increase in DI rats (p < 0.01 vs. LE). The basal hypothalamic content of CRH and catecholamines (epinephrine, norepinephrine, and dopamine) was similar in DI and LE rats. The hypothalamic AVP content in LE rats was unaffected by central HA infusion or restraint stress and was undetectable in DI rats. We conclude that inherited lack of AVP impaired the ACTH and β-END response to central HA administration as well as to restraint stress, suggesting that AVP is important for the mediation of these responses.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 82%

Impaired Histamine- and Stress-Induced Secretion of ACTH and β-Endorphin in Vasopressin- Deficient Brattleboro Rats

Kjær¹,

Knigge²,

Bach³

et al. 1993

Neuroendocrinology

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“…Moreover, both the polyclonal antibody employed in the present study and the N-terminal lipocortin fragment (LCI have been shown to modulate thermogenesis (65) and ischaemic damage (66, 67) when given centrally. Since histamine elicits the release of both CRF-41 and AVP from the hypothalamus (64) it is also possible, in view of our in vitro findings, that any inhibitory effect of LCI on CRF-41 secretion was masked by a concomitant rise in AVP release. Indeed, an increase in AVP release may explain the potentiation of the adrenocortical response to histamine observed in vivo with the lowest dose of LCI.…”

Section: Discussionmentioning

confidence: 86%

Effects of Lipocortin 1 and Dexamethasone on the Secretion of Corticotrophin‐Releasing Factors in the Rat: in vitro and in vivo Studies

Loxley

Cowell

Flower

et al. 1993

J Neuroendocrinology

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Lipocortin 1 (LC1: also called annexin 1) was first described as a putative second messenger protein for the anti-inflammatory steroids in peripheral tissues. In the present study, in vitro and in vivo methods were used to examine its potential role within the hypothalamus as a mediator of the regulatory actions of the glucocorticoids on the hypothalamo-pituitary-adrenocortical axis of the rat. In the in vitro studies, the effects of human recombinant LC1 (hu-r-LC1) on the concomitant release of the two major corticotrophin-releasing factors (CRF-41 and arginine vasopressin, AVP) from isolated hypothalami removed from chronically adrenalectomized rats were compared with those of dexamethasone in the presence and absence of appropriate secretagogues, namely phospholipase A2 (PLA2), interleukin-6 (IL-6) and a non-specific depolarizing agent, K+ (56 mM). The spontaneous release of CRF-41 in vitro was unaffected by either hu-r-LC1 (5 to 100 ng/ml) or dexamethasone (1 microM). Both compounds however reduced the release of the neuropeptide evoked by IL-6 (5 ng/ml) but failed to modify the secretory responses to PLA2 (25 U/ml) or K+ (56 mM). Dexamethasone (1 microM) had no effect on the basal release of AVP but effectively blocked the secretion of the peptide induced by either IL-6 (10 ng/ml) or PLA2 (25 U/ml). In complete contrast, hu-r-LC1 (5 to 100 ng/ml) stimulated the release of AVP and potentiated the secretory responses to IL-6 (10 ng/ml) and PLA2 (25 U/ml) but not to K+ (56 mM). The hypothalamic responses to PLA2 stimulation (25 U/ml) were associated with significant (P < 0.01) increases in prostaglandin E2 release which, in some instances, were potentiated by hu-r-LC1 (5 to 20 ng/ml). In vivo, administration of histamine (0.6 mg/100 g body wt, ip) produced significant (P < 0.01) increases in the serum corticosterone concentration and in the hypothalamic LC1 content. Neither hu-r-LC1 (0.6 to 1.2 micrograms) nor a polyclonal anti-LC1 antibody (3 microliters, diluted 1:200), injected intracerebroventricularly (icv), influenced either the resting serum corticosterone concentration or the hypersecretion of the steroid evoked by histamine stress. A lower dose of the recombinant protein (0.3 micrograms icv) also failed to alter basal corticosterone release but, in contrast to the higher doses, potentiated the pituitary-adrenocortical responses to histamine. The results suggest that LC1 may contribute to some aspects of peptide release in the hypothalamus but that its actions are not necessarily related to those of the glucocorticoids.

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“…Arginine vasopressin (AVP) has been reported to mediate suppressive effects of stress on LH secretion ( 16), and to play a role in compensation for the CRH deficiency ( 17). In addition, AVP and CRH synergistically stimulate corticotropin release from the isolated perfused anterior pituitary cells ( 18).…”

Section: Discussionmentioning

confidence: 99%

Effect of Corticotropin‐Releasing Hormone Antagonist on Oestrogen‐Dependent Glucoprivic Suppression of Luteinizing Hormone Secretion in Female Rats

Tsukahara

Tsukamura

Foster

et al. 1999

J Neuroendocrinology

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Pharmacological reduction of glucose availability with 2-deoxyglucose (2DG) suppresses pulsatile luteinizing hormone (LH) secretion in rats and growth-retarded lambs. Gonadal steroids enhance the glucoprivic suppression of LH secretion in rats. The present study determined if corticotropin-releasing hormone (CRH) plays a role in mediating oestrogen-dependent and -independent glucoprivic suppression of LH secretion. The study was conducted in ovariectomized (OVX) rats some of which received Silastic implants containing oestradiol-17beta (OE2) dissolved in peanut oil at 20 microg/ml to produce a physiological plasma level of OE2 (30 pg/ml). Seven days after ovariectomy, the rats were stereotaxically implanted with a guide cannula into the third cerebral ventricle. Seven days later, blood samples were collected through an indwelling atrial cannula every 6 min for 3 h for LH pulse determination. After the first hour of blood sampling, a CRH antagonist, [D-Phe12, Nle21,38]hCRF-(21-41), or vehicle was injected into the third cerebral ventricle through the implanted cannula before 2DG administration through the indwelling atrial cannula. Pulsatile LH secretion was suppressed by 2DG (200 mg/kg b.w.) in the vehicle-treated rats bearing OE2 implants. The CRH antagonist (5.65 nmol) blocked the suppressive effect of 2DG on pulsatile LH secretion in the OE2-treated OVX animals. On the other hand, in the absence of oestrogen, the effect of a twice greater dose of 2DG (400 mg/kg b.w.) was not blocked by five times greater amount of CRH antagonist (28.3 nmol). These results suggest the mechanisms mediating glucoprivic suppression of LH secretion involve two components: one is oestrogen-dependent and the other oestrogen-independent. CRH may be involved in the oestrogen-dependent component of glucoprivic suppression of LH secretion but not the oestrogen-independent one.

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A Role for Vasopressin in the Stress‐Induced Inhibition of Gonadotrophin Secretion: Studies in the Brattleboro Rat

Cited by 9 publications

References 41 publications

Impaired Histamine- and Stress-Induced Secretion of ACTH and β-Endorphin in Vasopressin- Deficient Brattleboro Rats

Impaired Histamine- and Stress-Induced Secretion of ACTH and β-Endorphin in Vasopressin- Deficient Brattleboro Rats

Effects of Lipocortin 1 and Dexamethasone on the Secretion of Corticotrophin‐Releasing Factors in the Rat: in vitro and in vivo Studies

Effect of Corticotropin‐Releasing Hormone Antagonist on Oestrogen‐Dependent Glucoprivic Suppression of Luteinizing Hormone Secretion in Female Rats

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