Regulation of Corticotrophin Secretion

Donald, R. A.; Sl, Alexander; Mj, Ellis; Mj, Evans; Jh, Livesey; Espiner, E. A.

doi:10.1042/cs0880004

Cited by 4 publications

(6 citation statements)

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“…Even in an absence of change in osmolality, physical stress normally results in a rise in AVP secretion secondary to increased hypothalamic-pituitary-adrenal axis activity (24). In this study, we showed that patients with central DI could not secrete copeptin in situations of psychological stress.…”

Section: Discussionmentioning

confidence: 61%

Copeptin concentrations during psychological stress: the PsyCo study

Siegenthaler

Walti

Urwyler

et al. 2014

European Journal of Endocrinology

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Objective: The prognostic/diagnostic biomarker copeptin, an arginine vasopressin surrogate, reflects physical stress. Whether copeptin concentration increases upon psychological stress is unknown. We investigated psychological stress effects on copeptin secretion in healthy volunteers and patients with central diabetes insipidus (DI). Design: A prospective observational study was conducted to study the relation between copeptin concentration and psychological stress. Methods: A total of 20 healthy adults (ten female) and eight patients with central DI (four female) underwent the Trier Social Stress Test including, in order, 30-min waiting period, 10-min anticipation period, 10-min test period and 40-min recovery. Serum copeptin and cortisol concentrations and self-rated stress component feelings were determined in the pre-/postanticipation period, post-test period and twice post-recovery. Results: In healthy volunteers, the median (25th-75th percentile) copeptin concentration peaked immediately during the post-test period at 5.1 (3.2-7.0) pmol/l, vs 3.7 (2.6-5.4) pmol/l at baseline. Over the measurement course, copeptin concentration significantly elevated (coefficient; 95% CI) (0.14; 0.06-0.23, PZ0.002). The important predictors of increase in copeptin concentration were feelings of tension (0.06; 0.04-0.08, P!0.001) and avoidance (0.07; 0.04-0.10; P!0.001). Copeptin and cortisol levels were associated (0.43; 0.13-0.72, P!0.005). Patients with DI had lower baseline concentrations (1.55 (1.2-3.1) pmol/l) when compared with healthy volunteers, PZ0.006. Patients with DI showed no increase upon psychological stress (peak 2.15 pmol/l (1.5-2.28), PZ0.79). By contrast, cortisol values were similar in patients and volunteers. Conclusions: In healthy volunteers, copeptin levels significantly increased after psychological stress testing; this response was blunted in patients with DI.

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Section: Discussionmentioning

confidence: 61%

Copeptin concentrations during psychological stress: the PsyCo study

Siegenthaler

Walti

Urwyler

et al. 2014

European Journal of Endocrinology

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“…It is known that CRH and AVP can be differentially regulated, even though they are, at least partially, colocalized ( 55). Considerable evidence from human studies measuring peripheral CRH and AVP levels as well as from studies on pituitary venous samples obtained in the horse suggest that AVP and CRH responses have a different response pattern to a variety of stimuli ( 56). Alternatively, the dissociation of AVP and CRH secretion may suggest that we are looking at a pool of AVP neurones distinct from those costoring CRH, but nevertheless involved in the regulation of the HPA axis.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Growth Hormone Secretagogues and Neuropeptide Y on Hypothalamic Hormone Release from Acute Rat Hypothalamic Explants

Korbonits

Little

Forsling

et al. 1999

J Neuroendocrinology

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Growth hormone (GH) secretagogues (GH-releasing peptides and their non-peptide analogues) stimulate growth hormone release via specific G-protein coupled receptors both directly from the pituitary gland and through stimulation of the hypothalamus. The exact mechanism of action in the hypothalamus is not known. The presence of endogenous GH releasing hormone (GHRH) seems to be necessary for the in-vivo actions of growth hormone secretagogues (GHSs), but data suggest that further factors must be involved as well. The effect of GHSs is not entirely specific for the GH axis; they release prolactin and stimulate the hypothalamo-pituitary-adrenal axis causing elevations in circulating ACTH and cortisol levels in both animal and human studies. Recently, it has also been suggested that GHSs stimulate hypothalamic neuropeptide Y (NPY) neurones. In the present study, we have therefore investigated the direct effect of several GHSs (GHRP-6, hexarelin and the non-peptide analogues L-692, 429 and L-692, 585) on GHRH, somatostatin (SS), corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) release in vitro in an acute rat hypothalamic incubation system. We also assessed the effect of NPY on GHRH, SS and AVP release. Freshly removed hypothalami were incubated in control media for 20 min and then in 1-4 consecutive 20-min periods in each of the test substances at different concentrations. There was no significant change in either the basal or potassium-stimulated release of GHRH or SS at low concentrations of any of the secretagogues; however, at millimolar doses a paradoxical inhibition of GHRH was observed with GHRP-6, hexarelin and L-692 585 (data are expressed as the ratio of treated to preceding basal release; at 20 min control group: 0.97+/-0.02, GHRP-6: 0.55+/-0.04, P<0.001 compared to control group; hexarelin: 0. 56+/-0.06, P<0.001, L-692,585: 0.70+/-0.03, P<0.001), while SS was stimulated after 60 or 80 min (at 80 min control: 0.80+/-0.03, hexarelin: 1.23+/-0.07, P<0.05 and L-692,585: 1.37+/-0.11, P<0.05). GHSs stimulated hypothalamic AVP release (at 20 min control: 0. 99+/-0.06 ratio to basal release, 10-4 M concentration of GHRP-6: 6. 31+/-1, P<0.001, hexarelin: 1.88+/-0.4, P<0.01, L-692,429: 1.90+/-0. 5, P<0.05 and L-692,585: 2.34+/-0.96, P<0.01), while no stimulatory effect was found on CRH release. NPY significantly stimulated SS and inhibited basal and potassium-stimulated GHRH release, while potentiating potassium-evoked AVP secretion. The Y1 receptor antagonist BIBP 3226 did not inhibit the effects of NPY on SS, GHRH or AVP release. We therefore conclude that, in this in-vitro rat hypothalamic incubation model, growth hormone secretagogues stimulate the release of AVP but have no effect on either GHRH, SS or CRH at low doses; at high doses paradoxically they inhibit the hypothalamic GH axis similar to in-vivo data in the rat. We speculate that these effects might be mediated by NPY.

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“…It has been shown that arginine vasopressin (AVP) has a regulatory effect on anterior pituitary function mainly by stimulating corticotropin (adrenocorticotropic hormone; ACTH) from the anterior pituitary, followed by an increase in cortisol response. AVP also acts synergistically with corticotropin‐releasing hormone (CRH) 1–4 . Even without a change in plasma osmolality, stress, pain, hypoxia, hypoglycemia and hypercapnia all result in an increase in AVP secretion, associated with an increase in the activity of the hypothalamus–pituitary–adrenal axis 1,3 .…”

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confidence: 99%

“…AVP also acts synergistically with corticotropin‐releasing hormone (CRH) 1–4 . Even without a change in plasma osmolality, stress, pain, hypoxia, hypoglycemia and hypercapnia all result in an increase in AVP secretion, associated with an increase in the activity of the hypothalamus–pituitary–adrenal axis 1,3 . In conditions that precipitate stress such as burns or surgical intervention, transitory increases have been noted in levels of AVP, ACTH and cortisol 5,6 .…”

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confidence: 99%