Cortisol release in pigs following peripheral and central administration of ovine and human corticotropin-releasing hormone

1990 ◽  
Vol 123 (1) ◽  
pp. 108-112 ◽  
Author(s):  
R. F. Parrott
Keyword(s):  
Plasma Cortisol ◽  
Behavioural Response ◽  
Route Of Administration ◽  
Cortisol Response ◽  
Cortisol Secretion ◽  
Intracerebroventricular Administration ◽  
Central Administration ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Cortisol Release

Abstract. Prepubertal pigs (N = 6) were surgically implanted with iv and intracerebroventricular catheters. The animals were given oCRH or hCRH peripherally (0, 20 or 50 μg) or centrally (0, 10 or 20 μg) and the effect on plasma cortisol measured. Peak cortisol concentrations were observed 20 min after iv, and 40 min after intracerebroventricular, administration. A larger cortisol response was observed when 20 μg oCRH was given by the central, compared to the peripheral, route and intracerebroventricular administration of both 10 and 20 μg oCRH caused excitation and vocalisation. By contrast, the effect of hCRH on cortisol secretion was small, regardless of the route of administration, and only one animal displayed a behavioural response when the highest dose was given centrally.

The corticotropin-releasing hormone test in normal short children: comparison of plasma adrenocorticotropin and cortisol responses to human corticotropin-releasing hormone and insulin-induced hypoglycemia

1989 ◽  
Vol 120 (3) ◽  
pp. 390-394 ◽  
Author(s):  
Katsumi Goji
Keyword(s):  
Plasma Cortisol ◽  
Response Curve ◽  
Cortisol Response ◽  
Corticotropin Releasing Hormone ◽  
Plasma Acth ◽  
Releasing Hormone ◽  
Short Children ◽  
The Mean ◽  
Maximum Increment ◽  
Peak Value

Abstract. The human corticotropin-releasing hormone (hCRH) tests were performed in twelve normal short children, and the responses of plasma ACTH and cortisol to iv administration of 1 μg/kg hCRH were compared with those to insulin-induced hypoglycemia. After administration of hCRH, the mean plasma ACTH level rose from a basal value of 3.3 ± 0.4 pmol/l (mean ± sem) to a peak value of 9.2 ± 0.8 pmol/l at 30 min, and the mean plasma cortisol level rose from a basal value of 231 ± 25 nmol/l to a peak value of 546 ± 30 nmol/l at 30 min. The ACTH response after insulin-induced hypoglycemia was greater than that after hCRH administration; the mean peak level (P < 0.01), the percent maximum increment (P < 0.01), and the area under the ACTH response curve (P < 0.01) were all significantly greater after insulin-induced hypoglycemia than those after hCRH administration. Although the mean peak cortisol level after insulin-induced hypoglycemia was about 1.3-fold higher than that after hCRH administration (P < 0.01), neither the percent maximum increment in plasma cortisol nor the area under the cortisol response curve after insulin-induced hypoglycemia was significantly different from that after hCRH administration. Consequently, the acute increases in plasma ACTH after the administration of 1 μg/kg hCRH stimulated the adrenal gland to almost the same cortisol response as that obtained with a much greater increase in plasma ACTH after insulin-induced hypoglycemia. These results suggest that a plasma ACTH peak of 9–11 pmol/l produces near maximum acute stimulation of adrenal steroidgenesis.

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.

Autoantibodies reacting with vasopressin and oxytocin in relation to cortisol secretion in major depression

2011 ◽  
Vol 26 (S2) ◽  
pp. 904-904
Author(s):  
F.D. Garcia ◽  
Q. Coquerel ◽  
E. Kiive ◽  
P. Déchelotte ◽  
J. Harro ◽  
...  
Keyword(s):  
Major Depression ◽  
Physical Exercise ◽  
Plasma Levels ◽  
Plasma Cortisol ◽  
Cortisol Response ◽  
Cortisol Secretion ◽  
Mild Depression ◽  
Moderate Depression ◽  
Before And After ◽  
Underlying Mechanisms

IntroductionAbnormal vasopressin (VP) and oxytocin (OT) signaling may contribute to the altered activity of the hypothalamo-pituitary-adrenal (HPA) axis in major depression; the underlying mechanisms remain uncertain.ObjectiveThis study characterized plasma levels and affinities of OT-and VP-reactive autoantibodies (autoAbs) with relation to disease severity and plasma cortisol response to physical exercise in patients with mild and moderate depression and healthy controls.MethodsPhysical exercise was used to elicit plasma cortisol response in 23 male depressive and 20 healthy subjects. All subjects were evaluated by the MADRS. Plasma levels VP-and OT-reactive IgG, IgA and IgM autoAbs were measured by ELISA, before and after the exercise, and affinity was measured by plasmon resonance.ResultsPlasma levels of OT-and VP-reactive total IgG autoAbs were lower in patients with moderate depression vs. controls and patients with mild depression. Both OT- and VP- free IgG autoAbs levels were negatively correlated with MADRS scores. Affinity values displayed 100 fold variability in both groups. Patients with moderate depression displayed blunted response of cortisol secretion to physical exercise. Baseline levels of VP total IgG and IgM autoAbs correlated negatively and of VP free IgG autoAbs correlated positively with plasma cortisol after physical exercise.ConclusionThese data show that changes of levels but not affinity of OT- and VP- reactive autoantibodies can be associated with the altered mood in subjects with moderate depression and that levels of VP-reactive autoAbs are associated with cortisol secretion.

Brain oxytocin receptors mediate corticotropin-releasing hormone-induced anorexia

1991 ◽  
Vol 260 (2) ◽  
pp. R448-R452 ◽  
Author(s):  
B. R. Olson ◽  
M. D. Drutarosky ◽  
E. M. Stricker ◽  
J. G. Verbalis
Keyword(s):  
Food Intake ◽  
Adrenocorticotropic Hormone ◽  
Central Administration ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Oxytocin Receptors ◽  
Artificial Cerebrospinal Fluid ◽  
Pituitary Secretion ◽  
Inhibit Food Intake ◽  
Stimulation Of

Central administration of corticotropin-releasing hormone (CRH) is known to inhibit food intake and stimulate pituitary oxytocin (OT) secretion in rats. These experiments addressed the possibility that the inhibition of food intake that follows central CRH administration is mediated through oxytocinergic pathways. Male food-deprived rats, with stable baseline food intakes after intracerebroventricular (icv) injections of artificial cerebrospinal fluid, received 150 pmol of CRH icv. Food intake was inhibited by 62 +/- 5% during a 90-min test period. Pretreatment with 9 nmol of the OT antagonist [d(CH2)5, Tyr(Me)2, Orn8]vasotocin icv completely eliminated the inhibition of food intake produced by icv CRH. In contrast, pretreatment with the OT-receptor antagonist did not significantly alter pituitary secretion of adrenocorticotropic hormone and OT stimulated by icv CRH. The results of these experiments implicate OT as a possible central mediator of CRH-induced anorexias in rats, particularly those that are accompanied by stimulation of neurohypophysial OT secretion.

scholarly journals Tail Docking of Piglets 2: Effects of Meloxicam on the Stress Response to Tail Docking

Animals ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1699
Author(s):  
Rebecca Morrison ◽  
Paul Hemsworth
Keyword(s):  
Stress Response ◽  
Plasma Cortisol ◽  
Acute Stress ◽  
Behavioural Response ◽  
Cortisol Response ◽  
Total Plasma ◽  
Sham Treatment ◽  
Commercial Viability ◽  
Tail Docking ◽  
Acute Stress Response

This experiment assessed the efficacy of the cauterisation procedure with or without pain relief (injectable meloxicam) in mitigating the acute stress response to tail docking. Male piglets (n = 432) were allocated to the following treatments at 2-d post-farrowing: (1) no handling, (2) sham handling, (3) tail docked using clippers, (4) tail docked using a cauteriser, (5) meloxicam + clipper, and (6) meloxicam + cauteriser. Meloxicam treatments used Metacam® at 5 mg/mL injected i.m. 1 h prior to tail docking. Blood samples were collected at 15 and 30 min post-treatment and analysed for total plasma cortisol. Behaviours indicative of pain such as escape attempts, vocalisations and standing with head lowered were measured. The duration of vocalisations and frequency of escape attempts during treatment were greater in all tail docking treatments compared to the sham treatment. Piglets in the clipper treatment had higher (p < 0.05) cortisol concentrations at 30 min but not 15 min after treatment and stood for longer (p < 0.001) with head lowered in the first 60 min after treatment than those in the cauterisation treatment. Meloxicam reduced (p < 0.05) both the cortisol response at 30 min after tail docking with the clipper as well as the behavioural response in the first 60 min after tail docking with the clipper. In comparison to the sham treatment, cortisol concentrations at 15 min were higher in the two tail docking treatments whereas the tail docking treatments with meloxicam were similar to the sham handling treatment. In comparison to the sham handling treatment, cortisol concentrations at 30 min post-docking were higher (p < 0.05) only in the clipper treatment. While cauterisation appears to be less aversive than the clipper procedure, the administration of meloxicam did not mitigate the behavioural response during tail docking using either procedure, but reduced standing with head lowered in the first hour after docking for both methods. The commercial viability of administration of meloxicam requires consideration before it is recommended for use compared to cauterisation alone, as it requires additional handling of piglets and costs.

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