Blockade of the V1b receptor reduces ACTH, but not corticosterone secretion induced by stress without affecting basal hypothalamic–pituitary–adrenal axis activity

Spiga, Francesca; Harrison, Louise; Wood, Susan A.; Knight, David; MacSweeney, Cliona; Thomson, Fiona; Craighead, Mark; Lightman, Stafford L.

doi:10.1677/joe-08-0421

Cited by 36 publications

(39 citation statements)

References 58 publications

(46 reference statements)

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“…It was surprising as AVP shows circadian rhythms of synthesis and release within the suprachiasmatic nucleus (Engelmann et al 1998), so its absence could have disturbed the daily rhythms of HPA axis hormone production as well. However, on the basis of the present results it seems that the lack of AVP in Brattleboro rats does not influence the pattern of the secretion, similar to results in V1b receptor KO mice (Lolait et al 2007a) and in rats given the V1b receptor antagonist (Spiga et al 2009). …”

Section: Discussionsupporting

confidence: 83%

“…In vitro studies show both that cAMP content (C; due to 5!10 K8 M CRH; nZ9-10) and ACTH secretion (D; due to 5-10 K11 M CRH; nZ10-11) were enhanced by CRH with a smaller ACTH response in di/di rats. found in studies using the V1b receptor antagonist (Org) in Sprague-Dawley rats (Spiga et al 2009) and in the V1b receptor KO mice (Stewart et al 2008), demonstrating that phenomenon is not species specific. The fact that the discrepancy between ACTH and corticosterone could not be explained by ACTH sensitivity or missed time points raises the possibility that other peripheral mediators are involved and may be acting directly on the adrenal gland.…”

Section: Discussionmentioning

confidence: 88%

“…A selective, non-peptide V1b receptor antagonist (SSR149415) was able to diminish the restraint-induced ACTH increased by 50% (Serradeil-Le Gal et al 2002) and inhibited the response to ether exposure but failed to inhibit the HPA axis response to forced swimming (Ramos et al 2006). Another V1b receptor antagonist (Org) diminished the restraint-and LPS-induced ACTH release without affecting the resting levels and stressinduced corticosterone responses (Spiga et al 2009).…”

Section: Introductionmentioning

confidence: 99%

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The stimuli-specific role of vasopressin in the hypothalamus–pituitary–adrenal axis response to stress

Zelena

Domokos

Jain

et al. 2009

Journal of Endocrinology

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Adaptation to a constantly changing environment is fundamental to every living organism. The hypothalamicpituitary-adrenocortical (HPA) axis is a key component of the adaptation process. The present study tests the hypothesis that vasopressin (AVP) is required for the HPA response to acute stimuli. To accomplish this, naturally AVP-deficient Brattleboro rats were exposed to a wide range of stimuli and their HPA response was compared with heterozygous littermattes. The circadian rhythmicity of plasma ACTH and corticosterone was not different between the two genotypes. The ACTH and corticosterone response to volume load, restraint or aggressive attack were decreased in AVP-deficient rats. The stress-induced increase in ACTH, but not corticosterone, was significantly impaired in AVPdeficient animals after novelty, elevated plus-maze, forced swim, hypoglycaemia, ulcerogenic cold immobilisation, lipopolysaccharide, hypertonic saline and egg white injection. The HPA response to social avoidance, ether inhalation and footshock was not different between the genotypes. In vitro, the hypophysis of AVP-deficient animals showed a reduction in stimulated ACTH production and their adrenal glands were hyporeactive to ACTH. A dissociation between the ACTH and corticosterone response was observed in several experiments and could not be explained by an earlier ACTH peak or enhanced adrenal sensitivity, suggesting the existence of paraadenohypophyseal neuroendocrine regulators. Loss of AVP affected the HPA response to a wide variety of stressors. Interestingly, the contribution of AVP to the HPA response was not specific for, nor limited to, a known stressor category. Thus, there is a context-specific requirement for AVP in stress-induced activation of the HPA axis.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

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The stimuli-specific role of vasopressin in the hypothalamus–pituitary–adrenal axis response to stress

Zelena

Domokos

Jain

et al. 2009

Journal of Endocrinology

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“…We have recently shown that this AVPR1B antagonist can reduce ACTH and corticosterone responses to exogenous AVP in rats (Spiga et al 2008). Furthermore, in the same report, we have shown that the same compound is able to reduce ACTH release induced by acute exposure to stress.…”

Section: Introductionsupporting

confidence: 52%

“…4). We have recently shown that this compound, injected 30 min prior to AVP, is able to reduce both ACTH and corticosterone response to AVP (Spiga et al 2008). Thus, this time point for Org administration in relation to both stress and AVP was used in the present study.…”

Section: Methodsmentioning

confidence: 99%

Effect of vasopressin 1b receptor blockade on the hypothalamic–pituitary–adrenal response of chronically stressed rats to a heterotypic stressor

Spiga¹,

Harrison²,

MacSweeney³

et al. 2008

Journal of Endocrinology

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Exposure to chronic restraint (CR) modifies the hypothalamicpituitary-adrenal (HPA) axis response to subsequent acute stressors with adaptation of the response to a homotypic and sensitization of the response to a heterotypic stressor. Since vasopressin (AVP) activity has been reported to change during chronic stress, we investigated whether this was an important factor in HPA facilitation. We therefore tested whether vasopressin 1b receptor (AVPR1B) blockade altered the ACTH and corticosterone response to heterotypic stressors following CR stress. Adult male rats were exposed to CR, single restraint, or were left undisturbed in the home cage. Twentyfour hours after the last restraint, rats were injected with either a AVPR1B antagonist (Org, 30 mg/kg, s.c.) or vehicle (5% mulgofen in saline, 0 . 2/kg, s.c.) and then exposed to either restraint, lipopolysaccharide (LPS) or white noise. CR resulted in the adaptation of the ACTH and corticosterone response to restraint and this effect was not prevented by pretreatment with Org. Although we found no effect of CR on LPS-induced ACTH and corticosterone secretion, both repeated and single episodes of restraint induced the sensitization of the ACTH, but not corticosterone response to acute noise. Pretreatment with Org reduced the exaggerated ACTH response to noise after both single and repeated exposure to restraint.

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Hypothalamus as an Endocrine Organ

Clarke

2014

Comprehensive Physiology

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The endocrine hypothalamus constitutes those cells which project to the median eminence and secrete neurohormones into the hypophysial portal blood to act on cells of the anterior pituitary gland. The entire endocrine system is controlled by these peptides. In turn, the hypothalamic neuroendocrine cells are regulated by feedback signals from the endocrine glands and other circulating factors. The neuroendocrine cells are found in specific regions of the hypothalamus and are regulated by afferents from higher brain centers. Integrated function is clearly complex and the networks between and amongst the neuroendocrine cells allows fine control to achieve homeostasis. The entry of hormones and other factors into the brain, either via the cerebrospinal fluid or through fenestrated capillaries (in the basal hypothalamus) is important because it influences the extent to which feedback regulation may be imposed. Recent evidence of the passage of factors from the pars tuberalis and the median eminence casts a new layer in our understanding of neuroendocrine regulation. The function of neuroendocrine cells and the means by which pulsatile secretion is achieved is best understood for the close relationship between gonadotropin releasing hormone and luteinizing hormone, which is reviewed in detail. The secretion of other neurohormones is less rigid, so the relationship between hypothalamic secretion and the relevant pituitary hormones is more complex.

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Blockade of the V1b receptor reduces ACTH, but not corticosterone secretion induced by stress without affecting basal hypothalamic–pituitary–adrenal axis activity

Cited by 36 publications

References 58 publications

The stimuli-specific role of vasopressin in the hypothalamus–pituitary–adrenal axis response to stress

The stimuli-specific role of vasopressin in the hypothalamus–pituitary–adrenal axis response to stress

Effect of vasopressin 1b receptor blockade on the hypothalamic–pituitary–adrenal response of chronically stressed rats to a heterotypic stressor

Hypothalamus as an Endocrine Organ

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