Corticotropin releasing factor activity of CRF 41 in normal man is potentiated by angiotensin II and vasopressin but not by desmopressin

Gaillard, Rolf C.; Riondel, A. M.; Ling, Nicholas; Müller, Alex F.

doi:10.1016/s0024-3205(88)80012-2

Cited by 37 publications

(21 citation statements)

References 47 publications

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“…In fact, evidence collected by us and others has demonstrated that most patients with Cushing's disease present a marked increase in plasma ACTH levels following i.v. administration of DDAVP (Malerbi et al 1993, Colombo et al 1997, Sakai et al 1997, Moro et al 2000, in contrast with the barely detectable response observed in normal subjects (Andersson et al 1972, Gaillard et al 1988 and patients with pseudoCushing syndrome (Malerbi et al 1996, Tsagarakis et al 1999, Coiro et al 2000, Moro et al 2000. On the basis of mRNA quantification studies, it had been hypothesized that the hyper-response observed in patients with Cushing's disease was due to an overexpression of the pituitary AVP receptor subtype (i.e.…”

Section: Discussionmentioning

confidence: 99%

“…This behaviour is typical for patients with an ACTH-secreting pituitary tumour as DDAVP exerts only a modest stimulatory effect in normal subjects (Andersson et al 1972, Gaillard et al 1988) and in patients with pseudoCushing syndrome (i.e. patients with alcoholism, obesity and depression, presenting clinical and/or biochemical features resembling Cushing's disease) (Malerbi et al 1996, Tsagarakis et al 1999, Coiro et al 2000, Moro et al 2000.…”

Section: Introductionmentioning

confidence: 99%

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Corticotrophin-releasing activity of desmopressin in Cushing's disease: lack of correlation between in vivo and in vitro responsiveness

Giraldi¹,

Marini²,

Torchiana³

et al. 2003

Journal of Endocrinology

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Desmopressin (DDAVP), an arginine vasopressin analogue, markedly stimulates ACTH secretion in patients with Cushing's disease, in contrast to its minimal effect in normal subjects. However, little is known about the mechanisms underlying this action and it appeared to be of interest to evaluate the effect of DDAVP on ACTHsecreting pituitary adenomas in vitro, in comparison with its effect in the same patients in vivo. Pituitary adenomas from 14 patients with Cushing's disease were incubated with DDAVP, corticotrophin-releasing hormone (CRH) and DDAVP together with vasopressin receptor antagonists or CRH. Incubation with DDAVP induced a modest dose-dependent increase in ACTH concentrations which appeared maximal at 10 nM. CRH stimulated ACTH to a greater extent compared with DDAVP and potentiated the effect of DDAVP alone. The DDAVP-induced ACTH increase appeared blunted by vasopressin V 2 and V 3 receptor antagonists. V 3 receptor gene expression was detected by RT-PCR in all adenoma samples except for two which were not responsive to DDAVP in vitro but responsive to the peptide in vivo. Surprisingly, no difference in the in vitro ACTH secretory response was observed between in vivo DDAVP-responsive (ACTH peak>150% baseline) and -unresponsive (ACTH peak<120% baseline) patients, suggesting that the pituitary adenoma is not the sole mediator of the ACTH-releasing effect of DDAVP. In conclusion, the marked stimulatory effect of DDAVP observed in patients with Cushing's disease appears to be mainly dependent on an extrapituitary action, possibly the inhibition of a corticotrophin release-inhibitory factor.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Corticotrophin-releasing activity of desmopressin in Cushing's disease: lack of correlation between in vivo and in vitro responsiveness

Giraldi¹,

Marini²,

Torchiana³

et al. 2003

Journal of Endocrinology

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“…Its action makes it a likely candidate for the observed activation of the HPA axis during critical illness. Other peptides involved in CRH and ACTH release which may be elevated during major stress include angiotensin-II (35) and neuropeptide-Y (36).…”

Section: Time (Min)mentioning

confidence: 99%

The hypothalamic-pituitary-adrenal axis in critical illness: response to dexamethasone and corticotropin-releasing hormone.

Reincke

Allolio

Würth

et al. 1993

The Journal of Clinical Endocrinology & Metabolism

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“…In normal conditions, AVP exerts its action by binding with two types of receptor: type VI, which is associated with the activation of cAMP and mediates pressor effects through vasoconstriction; and type V2, which mediates antidiuretic effects [19].The action which the hormone exerts on the corticotropic hypophyseal cells is attributed to the VI receptor by the majority of authors [19][20][21]. Some authors, however, maintain that the hypophyseal receptor for AVP is neither VI nor V2 [12];this could explain why DDAVP, which has no effect on the vessels and acts mainly as an antidiuretic through the V2 receptors, seems to exert a minimal effect on the corticotropic hypophyseal cells [13,15]. Some authors, however, maintain that the hypophyseal receptor for AVP is neither VI nor V2 [12];this could explain why DDAVP, which has no effect on the vessels and acts mainly as an antidiuretic through the V2 receptors, seems to exert a minimal effect on the corticotropic hypophyseal cells [13,15].…”

Section: Resultsmentioning

confidence: 99%

Differing responses of cortisol to oCRF during endonasal and oral treatment with DDAVP

Carraro

Giusti

Porcella

et al. 1994

Eur J Clin Investigation

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Arginine vasopressin (AVP) exerts a potentiating effect on the responses of cortisol and ACTH to ovine CRF (oCRF). A stimulation test using AVP plus oCRF to assess ACTH reserve has been proposed. In central diabetes insipidus, long-term substitution therapy is commonly undertaken with desmopressin (DDAVP), an analogue of the natural hormone which has a greater antidiuretic action but whose effects on the ACTH-cortisol axis are still controversial. The aim of our study was to evaluate the variations in the responses of ACTH and cortisol to oCRF in various phases of the treatment of central diabetes insipidus: no treatment, endonasal treatment with DDAVP solution and oral treatment with DDAVP in tablet form. Seven patients suffering from central diabetes insipidus underwent testing with oCRF during the various phases of treatment. In the absence of DDAVP treatment, normal responses were registered for cortisol (basal 164.1 +/- 29.4 ng ml-1, peak 396.1 +/- 37.9 ng ml-1; P < 0.05) and ACTH (basal 20.4 +/- 3.9 pg ml-1, peak 86.3 +/- 20.9 pg ml-1; P < 0.05) in all patients. During oral treatment with DDAVP, no variation in cortisol response to oCRF was seen. By contrast, when DDAVP was administered endonasally, a significant reduction in cortisol responsiveness to oCRF (secretory area: 2429 +/- 548 ng ml-1 120 min) was noted in comparison with that found during the other two tests (no treatment: 3070 +/- 704 ng ml-1 120 min; oral DDAVP: 3419 +/- 650 ng ml-1 120 min; P < 0.05) performed.(ABSTRACT TRUNCATED AT 250 WORDS)

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Corticotropin releasing factor activity of CRF 41 in normal man is potentiated by angiotensin II and vasopressin but not by desmopressin

Cited by 37 publications

References 47 publications

Corticotrophin-releasing activity of desmopressin in Cushing's disease: lack of correlation between in vivo and in vitro responsiveness

Corticotrophin-releasing activity of desmopressin in Cushing's disease: lack of correlation between in vivo and in vitro responsiveness

The hypothalamic-pituitary-adrenal axis in critical illness: response to dexamethasone and corticotropin-releasing hormone.

Differing responses of cortisol to oCRF during endonasal and oral treatment with DDAVP

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