Potentiation of the classic ovine corticotrophin releasing hormone stimulation test by the combined administration of small doses of lysine vasopressin

Favrod-Coune, Charles A.; Raux-Demay, Marie-Charles; Proeschel, M F; Bertagna, Xavier; Girard, François; Luton, J P

doi:10.1111/j.1365-2265.1993.tb00522.x

Cited by 30 publications

(12 citation statements)

References 33 publications

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“…Dose-response studies of intravenous AVP administration to normal humans have demonstrated that while a peripheral plasma AVP concentration of 60 pmol/1 does not stimulate ACTH and cortisol release [42], levels of 135 pmol/1 cause a significant rise in both ACTH and cortisol [43]. Considerably lower AVP concentrations of 5-10 pmol/1, achieved by hypertonic saline infusion, will augment the stimulatory effect of synthetic CRH in vivo [6,7], and this is consistent with reports that very low intra venous doses of AVP or LVP, which do not by themselves significantly increase ACTH levels above basal, still sub stantially increase the ACTH response to human or ovine 203 CRH [41,[44][45][46]. In the present study, plasma AVP levels were greater than 220 prnol/1 (considerably greater than the above threshold for ACTH release) 15 min prior to the peak ACTH responses (i.e., 10 min after AVP was admin istered) in all three tests in which active AVP was given.…”

Section: Discussionsupporting

confidence: 83%

A Synergistic Adrenocorticotropin Response to Naloxone and Vasopressin in Normal Humans: Evidence That Naloxone Stimulates Endogenous Corticotropin-Releasing Hormone

et al. 1995

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Naloxone stimulates pituitary-adrenal function by blocking an endogenous inhibitory opioidergic tone which modulates pituitary adrenocorticotropin (ACTH) release. In animals, this action of naloxone is mediated by increased corticotropin-releasing hormone (CRH) secretion, but such a mechanism is disputed in humans. CRH and arginine vasopressin (AVP) are known to have a synergistic effect on ACTH secretion in both humans and animals. In vitro, this synergism is independent of L-type voltage-dependent Ca²⁺ channel function. The aims of this study were therefore: (i) to determine if the combined administration of naloxone and AVP is synergistic regarding ACTH release; (ii) to assess the effect of nifedipine, which blocks L-type Ca²⁺ channels, on the ACTH response to combined naloxone/AVP stimulation. Seven healthy volunteers were studied using a placebo-controlled, single-blind protocol. Naloxone (125 µg/kg) and/or AVP (10 units) were given in all four possible combinations, and oral nifedipine (20 mg) was also given with naloxone and AVP as an additional test. The mean AUC and the mean peak change in ACTH levels following combined naloxone/AVP administration were both significantly greater than the arithmetic sum of the ACTH responses to naloxone and AVP given on separate occasions (AUC: 1,576.4 ± 417.9 vs. 567.1 ± 106.1 pmol·min·Hp < 0.002; peak change: 37.9 ± 14.0 vs. 11.8 ± 2.0ρmol/l, p < 0.007). Nifedipine reduced the ACTH response to combined naloxone/AVP stimulation by 43% (AUC: 1,576.4 ± 417.9 vs. 897.0 ± 186.2; p < 0.05), but it remained greater than the sum of the individual responses (897.0 ± 186.2 vs. 567.1 ± 106.1, p < 0.05). These results indicate that naloxone and AVP cause a synergistic ACTH response, and that this synergy is not abolished by nifedipine. They also provide evidence that naloxone stimulates the human hypothalamic-pituitary-adrenal axis predominantly or exclusively via increased release of endogenous CRH.

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Section: Discussionsupporting

confidence: 83%

A Synergistic Adrenocorticotropin Response to Naloxone and Vasopressin in Normal Humans: Evidence That Naloxone Stimulates Endogenous Corticotropin-Releasing Hormone

et al. 1995

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“…At the same time, some groups have reported that in the sheep AVP is the more potent secretagogue (Familari et al, 1989; Hassan et al, 2003). In all cases, a marked synergism between CRH and AVP has been observed (Antoni, 1993; Favrod-Coune et al, 1993; Aguilera et al, 1994; Aguilera, 1998; Serradeil-Le Gal et al, 2005). The impact of AVP on ACTH secretion is often regarded as ancillary to CRH as far as AVP alone is a weak ACTH secretagogue but acts synergistically with CRH to facilitate ACTH release both in humans (DeBold et al, 1984; Salata et al, 1988; Favrod-Coune et al, 1993) and rodents (Rivier and Vale, 1983; Antoni, 1993).…”

Section: Mechanisms Of Hpa Axis Regulationmentioning

confidence: 97%

“…In all cases, a marked synergism between CRH and AVP has been observed (Antoni, 1993; Favrod-Coune et al, 1993; Aguilera et al, 1994; Aguilera, 1998; Serradeil-Le Gal et al, 2005). The impact of AVP on ACTH secretion is often regarded as ancillary to CRH as far as AVP alone is a weak ACTH secretagogue but acts synergistically with CRH to facilitate ACTH release both in humans (DeBold et al, 1984; Salata et al, 1988; Favrod-Coune et al, 1993) and rodents (Rivier and Vale, 1983; Antoni, 1993). It has been shown that the corticotroph AVP/V1b and the CRH/CRHR1 signaling pathways converge to increase ACTH secretion (Abou-Samra et al, 1986; Roper et al, 2011).…”

Section: Mechanisms Of Hpa Axis Regulationmentioning

confidence: 97%

“…The ability of both neuropeptides CRH and AVP to stimulate the secretion of ACTH has been demonstrated in humans (DeBold et al, 1984; Salata et al, 1988; Favrod-Coune et al, 1993) and various other species, including non-human primates (Goncharova and Lapin, 2002; Goncharova, 2009a), rats (Vale et al, 1983; Antoni, 1993), mice (Muller et al, 2000; Lolait et al, 2007), horses (Evans et al, 1993), and sheep (McFarlane et al, 1995; Hassan et al, 2003). The relative importance of each seems to vary depending on the species.…”

Section: Mechanisms Of Hpa Axis Regulationmentioning

confidence: 99%

“…The relative importance of each seems to vary depending on the species. For example, in humans (DeBold et al, 1984; Favrod-Coune et al, 1993), non-human primates (Goncharova, 2009a), rats (Vale et al, 1983; Antoni, 1993; Serradeil-Le Gal et al, 2005), and horses (Evans et al, 1993), CRH is a much more potent secretagogue than AVP. At the same time, some groups have reported that in the sheep AVP is the more potent secretagogue (Familari et al, 1989; Hassan et al, 2003).…”

Section: Mechanisms Of Hpa Axis Regulationmentioning

confidence: 99%

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Stress Responsiveness of the Hypothalamic–Pituitary–Adrenal Axis: Age-Related Features of the Vasopressinergic Regulation

Goncharova¹

2013

Front. Endocrinol.

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The hypothalamic–pituitary–adrenal (HPA) axis plays a key role in adaptation to environmental stresses. Parvicellular neurons of the hypothalamic paraventricular nucleus secrete corticotrophin releasing hormone (CRH) and arginine vasopressin (AVP) into pituitary portal system; CRH and AVP stimulate adrenocorticotropic hormone (ACTH) release through specific G-protein-coupled membrane receptors on pituitary corticotrophs, CRHR1 for CRH and V1b for AVP; the adrenal gland cortex secretes glucocorticoids in response to ACTH. The glucocorticoids activate specific receptors in brain and peripheral tissues thereby triggering the necessary metabolic, immune, neuromodulatory, and behavioral changes to resist stress. While importance of CRH, as a key hypothalamic factor of HPA axis regulation in basal and stress conditions in most species, is generally recognized, role of AVP remains to be clarified. This review focuses on the role of AVP in the regulation of stress responsiveness of the HPA axis with emphasis on the effects of aging on vasopressinergic regulation of HPA axis stress responsiveness. Under most of the known stressors, AVP is necessary for acute ACTH secretion but in a context-specific manner. The current data on the AVP role in regulation of HPA responsiveness to chronic stress in adulthood are rather contradictory. The importance of the vasopressinergic regulation of the HPA stress responsiveness is greatest during fetal development, in neonatal period, and in the lactating adult. Aging associated with increased variability in several parameters of HPA function including basal state, responsiveness to stressors, and special testing. Reports on the possible role of the AVP/V1b receptor system in the increase of HPA axis hyperactivity with aging are contradictory and requires further research. Many contradictory results may be due to age and species differences in the HPA function of rodents and primates.

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Cushing's disease

et al. 2011

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Potentiation of the classic ovine corticotrophin releasing hormone stimulation test by the combined administration of small doses of lysine vasopressin

Abstract: Under these conditions, the combination of 100 micrograms CRH with 1 IU lysine vasopressin constitutes a powerful test for direct assessment of the pituitary reserve and therefore can be employed as a routine investigational tool.

Cited by 30 publications

References 33 publications

A Synergistic Adrenocorticotropin Response to Naloxone and Vasopressin in Normal Humans: Evidence That Naloxone Stimulates Endogenous Corticotropin-Releasing Hormone

A Synergistic Adrenocorticotropin Response to Naloxone and Vasopressin in Normal Humans: Evidence That Naloxone Stimulates Endogenous Corticotropin-Releasing Hormone

Stress Responsiveness of the Hypothalamic–Pituitary–Adrenal Axis: Age-Related Features of the Vasopressinergic Regulation

Cushing's disease

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