The diurnal variation of urinary and plasma 17-hydroxy-corticosteroid (17-OHCS) levels and the plasma 17-OHCS response to lysine-8- vasopressin in depressive patients

Jakobson, T; Blumenthal, Max; Hagman, Harriet; Heikkinen, Elsa

doi:10.1016/0022-3999(69)90006-3

Cited by 13 publications

(5 citation statements)

References 39 publications

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“…This observation which is consistent with the results of an earlier study [28] does not support the hypothesis that dexamethasone nonsup pression in depressed subjects is associated with de creased opioidergic tone or altered opiate receptor sensi tivity [29], In contrast to the failure of naloxone to induce cortisol escape, the administration of arginine vasopressin (3 units intravenously) produced an escape in 4 of 9 subjects. The variability in the cortisol response to vasopressin which is consistent with reports of large interindividual differences in the cortisol response to vasopressin of depressed and healthy subjects in the absence of dexamethasone pretreatment [16,18,21,23] could not be explained by differences in dexamethasone plasma levels but was associated with a decrease in sys tolic blood pressure. In agreement with the results of pre vious studies [17,21], we also failed to detect a relation ship between subjective discomfort symptoms and corti sol response to vasopressin.…”

Section: Discussionsupporting

confidence: 77%

“…These observations suggest that in addi tion to increased CRH production, changes in vasopres sin and/or opioidergic tone or alterations in receptor sensitivity to these peptides may be involved in the hypercortisolemia and/or dexamethasone nonsuppres sion present in depression. Relevant here are reports of altered cortisol response to vasopressin and decreased cortisol and prolactin responses to opiate agonists in depressed patients [16][17][18][19][20][21][22][23][24]. In order to further examine the possible role of endogenous opioid peptides and vasopressin in dexamethasone nonsuppression, we stud ied the effect of naloxone, arginine vasopressin, and vasopressin-naloxone combination on cortisol secretion in healthy male subjects pretreated with dexametha sone.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Vasopressin and Naloxone Alone and in Combination on Cortisol Secretion after Dexamethasone Pretreatment

Garland¹,

Zis²

1990

Horm Res

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In order to further examine the possible role of endogenous opioid peptides and vasopressin in the phenomenon of dexamethasone nonsuppression, we studied the effect of naloxone, vasopressin, and vasopressinnaloxone combination on cortisol secretion following dexamethasone pretreatment. Nine healthy males were given 1 mg dexamethasone at 23.00 h. The following day starting at 12.30 h and at 90-min intervals they received intravenously naloxone (0.2 mg/kg), arginine vasopressin 3 units, or the two drugs combined. The order of drug administration was counterbalanced using a Latin square design. Blood samples were drawn at 15-min intervals, and plasma aliquots were assayed for cortisol and dexamethasone. Naloxone failed to induce an escape from dexamethasone suppression. Four of the 9 subjects responded with an escape from dexamethasone suppression in response to vasopressin alone. The observed variability in response to vasopressin was unrelated to dexamethasone plasma levels but was associated with a decrease in systolic blood pressure. Peak cortisol levels were lowest in response to naloxone and highest in response to vasopressin. There was no evidence of an increased cortisol response to the coadministration of naloxone with vasopressin compared to vasopressin alone. These results fail to implicate an opioidergic mechanism in the pathophysiology of dexamethasone nonsuppression.

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Section: Discussionsupporting

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Effect of Vasopressin and Naloxone Alone and in Combination on Cortisol Secretion after Dexamethasone Pretreatment

Garland¹,

Zis²

1990

Horm Res

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“…Several groups have used vasopressin‐mediated cortisol output as a means of assessing HPA function in depressive disorders (Jakobsen et al. 1969; Carroll, 1972; Krahn et al.…”

Section: Vasopressin In Major Depressionmentioning

confidence: 99%

“…Several groups have used vasopressin-mediated cortisol output as a means of assessing HPA function in depressive disorders (Jakobsen et al 1969;Carroll, 1972;Krahn et al 1985). Although suggestive of an abnormal cortisol response to vasopressin administration, the results are difficult to interpret; two of the studies were uncontrolled and utilized lysine vasopressin, which causes significant adverse side-effects, and the third (Krahn et al 1985), although controlled, used small numbers and a submaximal dose of AVP.…”

Section: Vasopressin In Major Depressionmentioning

confidence: 99%

Anatomy of melancholia: focus on hypothalamic–pituitary–adrenal axis overactivity and the role of vasopressin

Dinan

Scott

2005

Journal of Anatomy

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Overactivity of the hypothalamic-pituitary-adrenal (HPA) axis characterized by hypercortisolism, adrenal hyperplasia and abnormalities in negative feedback is the most consistently described biological abnormality in melancholic depression. Corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) are the main secretagogues of the HPA/stress system. Produced in the parvicellular division of the hypothalamic paraventricular nucleus the release of these peptides is influenced by inputs from monoaminergic neurones. In depression, anterior pituitary CRH1 receptors are down-regulated and response to CRH infusion is blunted. By contrast, vasopressin V3 receptors on the anterior pituitary show enhanced response to AVP stimulation and this enhancement plays a key role in maintaining HPA overactivity.

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“…Patients with depressive illness often have both an abnormal plasma cortisol rhythm, and a high plasma cortisol level (Knapp et al 1967;Buller 8c Besser 1968;Fullerton et al 1968;Jakobson et al 1969). Patients with depressive illness often have both an abnormal plasma cortisol rhythm, and a high plasma cortisol level (Knapp et al 1967;Buller 8c Besser 1968;Fullerton et al 1968;Jakobson et al 1969).…”

Section: Discussionmentioning

confidence: 99%

Light Synchronization of the Circadian Rhythm of Plasma 11-Hydroxycorticosteroids in Man

Osterman

1974

Acta Endocrinologica

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The levels of plasma 11-hydroxycorticosteroids were studied in 4 healthy subjects with a constant sleep-waking cycle and a constant activity schedule before and after experimental alteration of the dark-light cycle. The subjects slept in the dark from 10.30 p. m. to 6.30 a. m. During a control period of 10 days the subjects stayed in rooms which were well lighted after 6.30 a. m. During the following 10 days darkness was prolonged by 4 h until 10.30 a. m. Hourly blood samples were obtained from 2.30 to 11.30 a.m. on days 9 and 10 of each period. Following the period of prolonged darkness there was a shift in the rhythm of the plasma 11\ x=r eq-\ hydroxycorticosteroids. The secretion period in the morning started later than during the control period. Present data indicate that in man the dark-light transition is important for the synchronization of the circadian plasma cortisol rhythm in the morning.

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The diurnal variation of urinary and plasma 17-hydroxy-corticosteroid (17-OHCS) levels and the plasma 17-OHCS response to lysine-8- vasopressin in depressive patients

Cited by 13 publications

References 39 publications

Effect of Vasopressin and Naloxone Alone and in Combination on Cortisol Secretion after Dexamethasone Pretreatment

Effect of Vasopressin and Naloxone Alone and in Combination on Cortisol Secretion after Dexamethasone Pretreatment

Anatomy of melancholia: focus on hypothalamic–pituitary–adrenal axis overactivity and the role of vasopressin

Light Synchronization of the Circadian Rhythm of Plasma 11-Hydroxycorticosteroids in Man

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