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.

Pituitary Adrenal Responsiveness to Corticotropin-Releasing Hormone in Chronic Uremic Patients

1990 ◽  
Vol 10 (2) ◽  
pp. 153-156 ◽  
Author(s):  
Kostas C. Siamopoulos ◽  
Mathew Dardamanis ◽  
Despina Kyriaki ◽  
Michael Pappas ◽  
George Sferopoulos ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Adrenocorticotropic Hormone ◽  
Acute Administration ◽  
Cortisol Response ◽  
Corticotropin Releasing Hormone ◽  
Plasma Acth ◽  
Normal Response ◽  
Releasing Hormone ◽  
Uremic Patients ◽  
Pituitary Adrenal Axis

We investigated the effect of exogenous ovine corticotropin-releasing hormone (oCRH) on plasma levels of adrenocorticotropic hormone (ACTH) and cortisol in 24 chronic renal failure patients: 8 nondialysis (NDCRF), 8 on hemodialysis (HD), and 8 on continuous ambulatory peritoneal dialysis (CAPD). In all groups the acute administration of oCRH caused a further increase (less pronounced in NDCRF patients) in the already elevated levels of cortisol. Following oCRH administration, plasma ACTH rose significantly in CAPD patients, but there was a blunted response of the hormone in the NDCRF and HD groups. The patterns of the ACTH and cortisol response in the last two groups, resemble those observed in chronic stress. We conclude that the hypothalamic-pituitary-adrenal axis in chronic uremic patients, retains the ability to respond to exogenous oCRH. Patients on CAPD, however, display a better, identical to normal response, which can be due to less chronic stress andlor to the more effective clearance of uremic toxins.

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.

scholarly journals GH and cortisol rebound rise during and following a somatostatin infusion: studies in dogs with the use of a GH-releasing peptide

2002 ◽  
Vol 174 (3) ◽  
pp. 387-394 ◽  
Author(s):  
AE Rigamonti ◽  
SM Bonomo ◽  
SG Cella ◽  
EE Muller
Keyword(s):  
Hpa Axis ◽  
Plasma Cortisol ◽  
Cortisol Response ◽  
Marked Rise ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Combined Administration ◽  
Cortisol Responses ◽  
Plasma Gh

GH-releasing peptides (GHRPs), a class of small synthetic peptide and non-peptide compounds, act on specific receptors at both the pituitary and the hypothalamic level to stimulate GH release in both humans and other animals. GHRPs, like corticotropin-releasing hormone (CRH), also possess acute ACTH- and cortisol-releasing activity, although the mechanisms underlying the stimulatory effect of GHRPs on the hypothalamo-pituitary-adrenal (HPA) axis are still unclear. In recent years, studies in humans and other animals have provided evidence that the rebound GH rise which follows withdrawal of an infusion of somatostatin (SS) (SSIW) is due, at least in part, to the functional activation of GH-releasing hormone (GHRH) neurons of the recipient organism. Unexpectedly, in humans, SS infusion, at a dose inhibiting basal GH secretion, has been associated with an activation of the HPA axis, leading to the hypothesis that this response was mediated, at least in part, by a central nervous system ACTH-releasing mechanism activated by the SS-induced decrease in GH secretion. Interestingly, the rebound GH rise which follows SSIW was magnified by the administration, before SS withdrawal, of a GHRP, implying that the SSIW approach could also be exploited to investigate in vivo the functional interaction in the process of GH and/or ACTH/cortisol secretion between endogenous GHRH (and/or other ACTH-releasing mechanisms) and GHRPs. In the present study, six young beagle dogs were given, on different occasions, at the beginning and at the end of a 3-h i.v. infusion of SS or saline (SAL), a bolus of physiological SAL or a GHRP compound, EP51216. SSIW induced a GH rebound rise without affecting plasma cortisol concentrations, while the withdrawal of SAL infusion was ineffective on either hormone paradigm. Administration of EP51216 at the beginning of SAL infusion evoked release of both GH and cortisol, whereas EP51216 administration at the withdrawal of SAL infusion evoked somatotroph and cortisol responses which were reduced in amplitude and duration. SS infusion significantly reduced the secretion of GH elicited by EP51216 but did not affect the rise of plasma cortisol levels. Interestingly, SSIW resulted in a marked enhancement of the somatotroph and cortisol responses evoked by EP51216. The marked rise of plasma GH levels induced by the GHRP after SSIW recalled that occurring after acute combined administration of recombinant human GHRH and EP51216, implying that exogenously delivered GHRP had synergized with the endogenous GHRH release triggered by SSIW. In contrast, acute combined administration of GHRH and the GHRP induced a cortisol response not different from that induced by GHRP alone, indicating that endogenous GHRH release was not involved in the enhanced cortisol response following EP51216 administration after SSIW. Similarly, the direct involvement of endogenous CRH could be ruled out, since i.v. administration of ovine CRH after SSIW evoked cortisol peak levels not different from those evoked by CRH at the withdrawal of SAL infusion. In conclusion, enhancement of the GH response to EP51216 alone by SSIW, to an extent reminiscent of that following combined administration of GHRH and EP61216, reinforces the view that SSIW elicits release of endogenous GHRH. Further studies are indeed necessary for a better understanding of the mechanisms underlying the enhanced cortisol response, since from now on the involvement of endogenous GHRH or CRH can be ruled out.

Plasma levels of corticotropin-releasing hormone in hypothalamic—pituitary—adrenal disorders and chronic renal failure

1993 ◽  
Vol 128 (6) ◽  
pp. 503-507 ◽  
Author(s):  
Kozo Hashimoto ◽  
Tatsuya Nishioka ◽  
Yukiko Numata ◽  
Takashi Ogasa ◽  
Jingo Kageyama ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Plasma Levels ◽  
High Performance ◽  
High Plasma ◽  
Reversed Phase ◽  
Corticotropin Releasing Hormone ◽  
Hypothalamic Pituitary Adrenal ◽  
Releasing Hormone ◽  
The Mean

Plasma levels of corticotropin-releasing hormone (CRH) were measured in hypothalamic-pituitary-adrenal disorders and chronic renal failure to investigate the clinical significance of plasma CRH. The mean plasma CRH level in normal subjects (N=26) was 1.64±0.43 pmol/l (normal range 0.77–2.5 pmol/l). Four of six patients with hypothalamic disorders receiving hydrocortisone supplementation had a low plasma CRH level. Two of six patients with Sheehan's syndrome had a low plasma CRH level whereas one patient had a high plasma CRH level. Two patients with Cushing's syndrome had a low plasma CRH level whereas two patients with Cushing's disease had a normal plasma CRH level. Six of 19 patients receiving prednisolone therapy had a low plasma CRH level. The mean plasma CRH level in this group was 0.97±0.34 pmol/l, which is significantly lower than that in the normal group. In this group, significant correlation was seen between plasma CRH and adrenocorticotropin levels. Eleven of 21 patients with chronic renal failure undergoing hemodialysis had a high plasma CRH level. Just after hemodialysis the plasma CRH levels decreased in 15 of 20 patients, while plasma adrenocorticotropin and cortisol levels increased in 13 of 19 patients and in 15 of 20 patients, respectively. Immunoreactive CRH in plasma measured both before and after hemodialysis eluted similarly on reversed-phase high-performance liquid chromatography. These results suggest that the plasma CRH level is at least partially suppressed by a chronically elevated plasma glucocorticoid level and that CRH in plasma is partially removed by hemodialysis.

Plasma Cortisol Changes in Seawater-Adapted Mummichogs (Fundulus heteroclitus) Exposed to Ammonia

1989 ◽  
Vol 46 (12) ◽  
pp. 2065-2069 ◽  
Author(s):  
Stephen Spotte ◽  
Gary Anderson
Keyword(s):  
Plasma Cortisol ◽  
Fundulus Heteroclitus ◽  
Mean Value ◽  
Effective Concentration ◽  
Cortisol Concentration ◽  
Control Fish ◽  
Cortisol Response ◽  
Plasma Cortisol Concentration ◽  
The Mean ◽  
Temperature Constant

Seawater-adapted mummichogs (Fundulus heteroclitus) were exposed to total NH4-N concentrations of 1, 2, 5, 10, 25, 50, 100, 150, and 200 mg/L for periods of 2, 4, 8, 12, 18, 24, 36, and 48 h. Afterward, the fish were captured quickly and anesthetized with MS-222 before blood was collected. The concentration of total NH4-N and duration of exposure accounted for, respectively, ~35 and <4% of the observed increase in plasma cortisol. The effective concentration (the concentration of total NH4-N inducing a mean cortisol response two standard deviations above the mean of the controls) was 47.14 mg/L, corresponding with a mean cortisol level of 13.44 μg/dL. Test concentrations of NH3-N were calculated from total NH4-N, pH, salinity, and temperature (constant at 20 °C), and the effects of both forms of ammonia on plasma cortisol concentration were compared. Significance was not detected at p < 0.05, demonstrating that total NH4-N and NH3-N explained the observed changes in cortisol levels similarly. Mean cortisol concentrations of mummichogs anesthetized and sampled in the field were comparable with published values and did not differ significantly from the mean value of captive control fish sampled after the same length of time in MS-222 (p < 0.05).

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