Effect of naloxone on oxytocin-induced cortisol decrease in normal men

1985 ◽  
Vol 108 (2) ◽  
pp. 261-265 ◽  
Author(s):  
V. Coiro ◽  
P. Chiodera ◽  
G. Rossi ◽  
R. Volpi ◽  
M. Salvi ◽  
...  
Keyword(s):  
Inhibitory Control ◽  
Opioid Peptides ◽  
Plasma Cortisol ◽  
Inhibitory Action ◽  
Opioid Antagonist ◽  
Cortisol Secretion ◽  
Plasma Acth ◽  
Cortisol Levels ◽  
Normal Men ◽  
Cortisol Release

Abstract. iv administration of oxytocin decreases plasma ACTH-cortisol levels in normal men. In contrast, naloxone, a specific opioid antagonist, stimulates cortisol release, suggesting that opioid peptides exert an inhibitory control on ACTH-cortisol secretion. The present study was carried out in an attempt to determine whether an opioid pathway mediates oxytocin action; therefore, we evaluated the effect of naloxone on the decrease of cortisol induced by oxytocin. Six normal men were treated iv with oxytocin (2 IU as a bolus), naloxone (4 mg as a bolus plus 10 mg infused for 2 h) or a combination of the 2 drugs. Plasma cortisol levels were determined in samples taken before and 2 h after drug treatment. As expected, administration of oxytocin significantly decreased cortisol secretion, while naloxone had a stimulatory effect on plasma cortisol levels. When oxytocin injection was followed by administration of naloxone, cortisol levels remained unchanged; thus, naloxone abolished a cortisol decrement in response to oxytocin. These findings show that in man oxytocin requires an active opioid system in order to produce its inhibitory action on ACTH-cortisol secretion, suggesting that this effect of oxytocin could be mediated by an opioid pathway.

Cyclic Cushing's syndrome combined with cortisol suppressible, dexamethasone non-suppressible ACTH secretion: a new variant of Cushing's syndrome

1985 ◽  
Vol 110 (3) ◽  
pp. 289-295 ◽  
Author(s):  
Hans-Udo Schweikert ◽  
Horst Lorenz Fehm ◽  
Rudolf Fahlbusch ◽  
Rainer Martin ◽  
Rainer Kolloch ◽  
...  
Keyword(s):  
Cushing’S Syndrome ◽  
Normal Tissue ◽  
Plasma Cortisol ◽  
Cushing's Syndrome ◽  
Cortisol Secretion ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Normal Response ◽  
New Variant ◽  
Marked Suppression

Abstract. A 55 year old woman with an unusual form of Cushing's disease was studied. During several periods (periods lasting up to 84 days) evidence of cortisol hypersecretion with cycles occurring every 6 days was found. Suppression of plasma cortisol through orally administered dexamethasone (up to 32 mg per day) could not be achieved either during periods of cyclic cortisol hypersecretion or during apparent remission with normal cortisol secretion. Marked suppression of plasma ACTH was measured in response to an iv infusion of 50 mg cortisol over a period of 55 min whereas a similar test with 2 mg dexamethasone (iv bolus) did not suppress ACTH secretion. Transsphenoidal exploration of the sella revealed a tumour surrounding the anterior pituitary. Examination of the pituitary showed a few tiny tumour structures embedded in normal tissue which could not be removed, when the tumour was resected selectively under preservation of normal appearing tissue. Post-operatively, clinical and chemical remission (normal response to 1 mg dexamethasone) was observed for about 4 months. Thereafter, cortisol hypersecretion occurred again necessitating bilateral adrenalectomy. Our results are compatible with the assumption that normal hypothalamic-pituitary-adrenal suppressibility with cortisol, but not with dexamethasone, was caused by the loss of feedback receptors for dexamethasone in the presence of cortisol receptors in the cells which secrete ACTH or CRF. The combination of cyclic hypercortisolism with dexamethasone non-suppressible Cushing's syndrome has not been reported before and thus represents a new variant of Cushing's syndrome.

Reduced Testosterone Levels in Cluster Headache: A Stress-Related Phenomenon?

Cephalalgia ◽  
1986 ◽  
Vol 6 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Fabio Facchinetti ◽  
Giuseppe Nappi ◽  
Claudio Cicoli ◽  
Giuseppe Micieli ◽  
Michela Ruspa ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Cluster Headache ◽  
Plasma Cortisol ◽  
Active Phase ◽  
Early Morning ◽  
Related Phenomenon ◽  
Cortisol Secretion ◽  
Plasma Cortisol Concentration ◽  
Episodic Cluster Headache ◽  
Cortisol Levels

The circadian changes in testosterone (T) and cortisol secretion and morning luteinizing hormone (LH) levels were evaluated in nine episodic cluster headache (CH) patients in active phase and in seven healthy volunteers, with collection of blood samples every 2 h for 24 h. CH showed a significant reduction of the 24-h integrated mean T value (mesor) (4.4 + 1.1 ng/ml; x ± SD) in comparison with controls (6.6 ± 0.8 ng/ml) ( P < 0.0l). Both groups had plasma T circadian rhythm with peak values in early morning, but in CH single cosinor analysis showed its absence in three out of nine CH patients. The rhythm showed an acrophase delay of 101 min in CH. Both patients and controls had a significant circadian rhythm of plasma cortisol concentration. CH patients, however, showed an acrophase delay of 106 min and significantly increased concentrations from 1200 h to 2000 h. Morning LH values were similar in the two groups. The reduced secretion of plasma T in CH patients in the active phase coexisted with an acrophase delay of its circadian rhythm. A similar delay was found in 24-h plasma cortisol levels. We suggest that stress accompanying attack expectancy in the active phase is the mechanism behind the elevated plasma cortisol levels. This in turn could reduce T concentrations, acting at the testicular level. These disturbances in internal chronoorganization support the hypothesis that cluster headache is basically a dyschronic disorder.

INHIBITION BY DEXAMETHASONE OF ADRENOCORTICOTROPHIN AND CORTISOL RELEASE INDUCED BY INTRAVENOUS INFUSION OF ATP AND DIBUTYRYL CYCLIC AMP IN PIGLETS

1974 ◽  
Vol 60 (1) ◽  
pp. 65-73 ◽  
Author(s):  
D. B. COOK ◽  
G. V. GILL ◽  
I. M. D. JACKSON ◽  
G. A. SMART
Keyword(s):  
Cyclic Amp ◽  
Intravenous Infusion ◽  
Similar Pattern ◽  
Plasma Cortisol ◽  
Dibutyryl Cyclic Amp ◽  
Plasma Acth ◽  
Intravenous Infusions ◽  
Consistent Increase ◽  
Cortisol Release ◽  
Corticosteroid Response

SUMMARY The effect of intravenous infusions of ATP and dibutyryl cyclic AMP (DB cyclic AMP) on adrenocorticotrophin (ACTH) and corticosteroid release was investigated in piglets. A consistent increase of both plasma ACTH and plasma cortisol was observed in response to infusions of 600 mg ATP/h. These responses were abolished by pretreating the animals with dexamethasone. A similar pattern of response was observed with DB cyclic AMP infused intravenously. No response occurred when 100 mg DB cyclic AMP were infused in 1 h, but there was a marked plasma corticosteroid response to an infusion of 600 mg DB cyclic AMP in 1 h. Surprisingly, this response was also abolished by pretreatment with dexamethasone.

Effects of neuroleptic treatment on cortisol and 3-methoxy-4-hydroxyphenylethyl glycol levels in blood

1995 ◽  
Vol 144 (3) ◽  
pp. 425-429 ◽  
Author(s):  
G Wik
Keyword(s):  
Drug Treatment ◽  
Plasma Cortisol ◽  
Neuroleptic Drug ◽  
Cortisol Secretion ◽  
Healthy Controls ◽  
Neuroleptic Treatment ◽  
Before And After ◽  
Cortisol Levels

Abstract Plasma cortisol and serum 3-methoxy-4-hydroxyphenylethyl glycol (MHPG) were determined before and after 5–6 weeks of neuroleptic treatment in patients with schizophrenia. Following drug treatment both plasma cortisol and serum MHPG levels in patients decreased and plasma cortisol levels were also lower than in unmedicated healthy controls. Indications of a relationship between the reduction of cortisol and MHPG levels were found. The data show that neuroleptic drug treatment inhibits cortisol secretion. It is speculated that this inhibition could be related to reduced noradrenergic activity. Journal of Endocrinology (1995) 144, 425–429

scholarly journals Aberrant Membrane Hormone Receptors in Incidentally Discovered Bilateral Macronodular Adrenal Hyperplasia with Subclinical Cushing’s Syndrome

2001 ◽  
Vol 86 (11) ◽  
pp. 5534-5540 ◽  
Author(s):  
Isabelle Bourdeau ◽  
Pierre D’Amour ◽  
Pavel Hamet ◽  
Jean-Marie Boutin ◽  
André Lacroix
Keyword(s):  
Cushing’S Syndrome ◽  
Plasma Cortisol ◽  
Hormone Receptors ◽  
Gastric Inhibitory Polypeptide ◽  
Urinary Free Cortisol ◽  
Cushing's Syndrome ◽  
Cortisol Secretion ◽  
Adrenal Hyperplasia ◽  
Free Cortisol ◽  
Cortisol Levels

Cortisol secretion in adrenal Cushing’s syndrome can be regulated by the aberrant adrenal expression of receptors for gastric inhibitory polypeptide, vasopressin, catecholamines, LH/human CG (LH/hCG), or serotonin. Four patients with incidentally discovered bilateral macronodular adrenal hyperplasia without clinical Cushing’s syndrome were evaluated for the possible presence of aberrant adrenocortical hormone receptors. Urinary free cortisol levels were within normal limits, but plasma cortisol levels were slightly elevated at nighttime and suppressed incompletely after dexamethasone administration. Plasma ACTH was partially suppressed basally but increased after administration of ovine CRH. A 51-yr-old woman had ACTH-independent increases of plasma cortisol after 10 IU AVP im (292%), 100 μg GnRH iv (184%), or 10 mg cisapride orally (310%); cortisol also increased after administration of NaCl (3%), hCG, human LH, and metoclopramide. In a 61-yr-old man, cortisol was increased by AVP (349%), GnRH (155%), hCG (252%), and metoclopramide (191%). Another 53-yr-old male increased plasma cortisol after AVP (171%) and cisapride (142%). Cortisol secretion was also stimulated by vasopressin in a 54-yr-old female. This study demonstrates that subclinical secretion of cortisol can be regulated via the aberrant function of at least V1-vasopressin, LH/hCG, or 5-HT4 receptors in incidentally identified bilateral macronodular adrenal hyperplasia.

Elevated endogenous cortisol reduces autonomic neuroendocrine and symptom responses to subsequent hypoglycemia

2002 ◽  
Vol 282 (4) ◽  
pp. E770-E777 ◽  
Author(s):  
Veronica P. McGregor ◽  
Salomon Banarer ◽  
Philip E. Cryer
Keyword(s):  
Plasma Cortisol ◽  
Autonomic Failure ◽  
Plasma Norepinephrine ◽  
Cortisol Secretion ◽  
Vicious Cycle ◽  
Plasma Epinephrine ◽  
Autonomic Symptom ◽  
Endogenous Cortisol ◽  
Cortisol Responses ◽  
Cortisol Levels

We tested the hypothesis that increased endogenous cortisol secretion reduces autonomic neuroendocrine and neurogenic symptom responses to subsequent hypoglycemia. Twelve healthy young adults were studied on two separate occasions, once after infusions of a pharmacological dose of α-(1–24)-ACTH (100 μg/h) from 0930 to 1200 and 1330 to 1600, which raised plasma cortisol levels to ∼45 μg/dl on day 1, and once after saline infusions on day 1. Hyperinsulinemic (2.0 mU · kg−1· min−1) stepped hypoglycemic clamps (90, 75, 65, 55, and 45 mg/dl glucose steps) were performed on the morning of day 2 on both occasions. These markedly elevated antecedent endogenous cortisol levels reduced the adrenomedullary ( P = 0.004, final plasma epinephrine levels of 489 ± 64 vs. 816 ± 113 pg/ml), sympathetic neural ( P = 0.0022, final plasma norepinephrine levels of 244 ± 15 vs. 342 ± 22 pg/ml), parasympathetic neural ( P = 0.0434, final plasma pancreatic polypeptide levels of 312 ± 37 vs. 424 ± 56 pg/ml), and neurogenic (autonomic) symptom ( P = 0.0097, final symptom score of 7.1 ± 1.5 vs. 10.6 ± 1.6) responses to subsequent hypoglycemia. Growth hormone, but not glucagon or cortisol, responses were also reduced. The findings that increased endogenous cortisol secretion reduces autonomic neuroendocrine and neurogenic symptom responses to subsequent hypoglycemia are potentially relevant to cortisol mediation of hypoglycemia-associated autonomic failure, and thus a vicious cycle of recurrent iatrogenic hypoglycemia, in people with diabetes mellitus.

Pregnancy alters cortisol feedback inhibition of stimulated ACTH: studies in adrenalectomized ewes

2001 ◽  
Vol 280 (6) ◽  
pp. R1790-R1798 ◽  
Author(s):  
Maureen Keller-Wood ◽  
Charles E. Wood
Keyword(s):  
Plasma Cortisol ◽  
Feedback Inhibition ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Feedback Effects ◽  
Low Concentrations ◽  
Pregnancy And Postpartum ◽  
Cortisol Levels

These studies test the hypothesis that pregnancy alters the feedback effects of cortisol on stimulated ACTH secretion. Ewes were sham-operated (Sham), or adrenalectomized (ADX) at ∼108 days gestation and replaced with aldosterone (3 μg · kg−1· day−1) and with cortisol at either of two doses (ADX + 0.6 and ADX + 1 mg · kg−1· day−1); ewes were studied during pregnancy and postpartum. Mean cortisol levels produced in ADX ewes were similar to normal pregnant ewes (ADX+1) or nonpregnant ewes (ADX+0.6), respectively. Plasma ACTH concentrations in response to infusion of nitroprusside were significantly increased in the pregnant ADX+0.6 ewes (1,159 ± 258 pg/ml) relative to pregnant Sham ewes (461 ± 117 pg/ml) or the ADX+1 ewes (442 ± 215 pg/ml) or the same ewes postpartum (151 ± 69 pg/ml). Plasma ACTH concentrations were not significantly different among the groups postpartum. Increasing plasma cortisol to 20–30 ng/ml for 24 h before hypotension produced similar inhibition of ACTH in all groups. Pregnancy appears to decrease the effectiveness of low concentrations of cortisol to inhibit ACTH responses to hypotension.

scholarly journals Effect of leptin on ACTH-stimulated secretion of cortisol in rhesus macaques and on human adrenal carcinoma cells

1999 ◽  
pp. 534-538 ◽  
Author(s):  
J Lado-Abeal ◽  
JJ Mrotek ◽  
DM Stocco ◽  
RL Norman
Keyword(s):  
Rhesus Monkeys ◽  
Solid Phase ◽  
In Vivo Studies ◽  
Cortisol Secretion ◽  
Adrenal Carcinoma ◽  
H295r Cells ◽  
Cortisol Levels ◽  
Cortisol Release

OBJECTIVE: Because glucocorticoids stimulate leptin release and, at least in vitro, leptin inhibits cortisol secretion, a feedback system between glucocorticoids and leptin has been proposed. However, in humans and non-human primates there are no in vivo studies to support any role for leptin in the control of the hypothalamic-pituitary-adrenal axis. In this study, we investigated the effect of leptin on (i) ACTH-stimulated secretion of cortisol in six male rhesus monkeys and (ii) basal and forskolin (FSK)-stimulated cortisol secretion by the human adrenal carcinoma cell H295R in vitro. DESIGN AND METHODS: In vivo studies: after suppression of endogenous ACTH with either dexamethasone (n=6) or a corticotropin-releasing factor (CRF) antagonist (d-Phe CRF(12-41)) (n=3), 1 microg bolus of human ACTH(1-24) was administered to stimulate adrenal cortisol release. Blood samples were collected every 15 min for 3 h. Leptin (1 mg) was infused over 4 h, starting 1 h before ACTH bolus. In vitro studies: NCI-H295R cells were incubated for 6, 12, 24 and 48 h in the absence or presence of 20 micromol/l FSK in combination with leptin (100 ng/ml medium). Cortisol levels in serum and medium were measured by solid phase radioimmunoassay. RESULTS: Acute leptin infusion to rhesus monkeys did not change basal cortisol levels, peak cortisol levels after ACTH(1-24) or the area under the curve when compared with studies in which leptin was not given. FSK increased cortisol levels in medium at 24 and 48 h, but leptin did not change cortisol release in either control or FSK-stimulated cells. CONCLUSIONS: Short-term leptin infusion affected neither the cortisol response to ACTH in non-human primates in vivo nor cortisol release (basal or FSK stimulated) by H295R cells, in vitro. These data suggest that leptin may not be an acute regulator of primate adrenal cortisol secretion.

Effect of ovine corticotrophin releasing factor, bromocriptine, and dopamine on release of ACTH and β-endorphin in a patient with Cushing's disease

1985 ◽  
Vol 109 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Hiroko Nakashima ◽  
Yukio Hirata ◽  
Masahito Uchihashi ◽  
Masahiro Tomita ◽  
Takuo Fujita
Keyword(s):  
Pituitary Adenoma ◽  
Cushing’S Disease ◽  
Plasma Cortisol ◽  
Cushing's Disease ◽  
Intermediate Lobe ◽  
Plasma Acth ◽  
Corticotrophin Releasing Factor ◽  
Predominant Component ◽  
Cortisol Levels

Abstract. Release of immunoreactive ACTH and β-endorphin (β-EP) in response to corticotrophin-releasing factor (CRF) and dopaminergic agents was studied in vivo and in vitro in a patient with Cushing's disease. Iv administration of synthetic ovine (o) CRF significantly stimulated plasma ACTH release, accompanied by increase of plasma cortisol levels. Oral administration of bromocriptine significantly suppressed plasma cortisol levels. Although reduced responses of plasma ACTH and cortisol to o-CRF was observed 1 month after removal of the pituitary adenoma, these normalized 6 months after operation. In vitro perifusion of the pituitary adenoma obtained by surgery revealed that o-CRF also stimulated ACTH and β-EP release in a dose-responsive manner (10−9m–10−5 m) and that dopamine suppressed their basal secretion. Gel exclusion chromatography of the perfusates showed that the predominant component of ACTH and β-EP before and after o-CRF stimulation coeluted with standard ACTH and β-EP, respectively. The present data suggest that o-CRF is a potent secretagogue for ACTH and β-EP release from the human pituitary adenoma causing Cushing's disease and that ACTH secretion from certain adenomas, possibly originating from the intermediate lobe of the pituitary gland, is partly regulated by a dopaminergic mechanism.

scholarly journals Does road transport influence plasma leptin concentrations in horses? Preliminary study

2018 ◽  
Vol 18 (1) ◽  
pp. 185-193
Author(s):  
Witold Kędzierski ◽  
Zbigniew Bełkot
Keyword(s):  
Plasma Cortisol ◽  
Road Transport ◽  
Cortisol Concentration ◽  
Cortisol Secretion ◽  
Blood Samples ◽  
Plasma Cortisol Concentration ◽  
Preliminary Study ◽  
Plasma Leptin ◽  
Cortisol Release ◽  
Arrival Point

Abstract Transport is one of the most common stressors for horses leading to an increase in cortisol secretion. Cortisol promotes leptin synthesis and release. The aim of the study was to evaluate the effect of short transport on circulating leptin and cortisol concentrations. A total of 16 crossbred naïve horses (7 geldings, 9 mares) aged 2-11 years, and weighing 530-680 kg were included in the study. The horses were transported in a commercial horse-truck to an unknown holding pen for temporary housing. To measure plasma leptin and cortisol concentrations, three blood samples were collected from each horse: before transport, immediately after unloading from the truck, and nine hours after transport at the arrival point. Transport caused a significant increase in mean plasma cortisol concentration determined at unloading, and after nine hours of unloading, in comparison to values obtained before loading. Plasma leptin concentrations did not change during the study. In conclusion, transportation procedures did not influence plasma leptin concentration in horses, despite significantly increased cortisol release.

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