Relationship of nocturnal plasma bioactive and immunoactive ACTH concentrations to cortisol secretion in normal men

1989 ◽  
Vol 121 (6) ◽  
pp. 857-865 ◽  
Author(s):  
Russell E. Poland ◽  
Koichi Hanada ◽  
Robert T. Rubin
Keyword(s):  
Plasma Concentrations ◽  
Normal Male ◽  
Cortisol Secretion ◽  
Plasma Acth ◽  
Average Correlation ◽  
Adrenal Cell ◽  
Male Volunteers ◽  
Shared Variance ◽  
Normal Men ◽  
Relationship Of

Abstract. Plasma concentrations of ACTH and cortisol were measured at 15-min intervals from 22.30 to 07.00 h in 8 normal male volunteers. ACTH was measured both by a modified and sensitized isolated adrenal cell bioassay and by radioimmunoassay. Within-subject correlations between bioactive ACTH and cortisol concentrations ranged between 0.86 and 0.95, with an average correlation of 0.93 (86% shared variance). In contrast, within-subject correlations between immunoassayable ACTH and cortisol ranged between 0.03 and 0.92, with an average correlation of 0.69 (48% shared variance). These results suggest that plasma ACTH concentrations determined by RIA might not accurately reflect the capacity of plasma to regulate the secretion of adrenal glucocorticoids.

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.

Coordinate activation of the corticotropic axis by insulin-induced hypoglycemia: simultaneous estimates of β-endorphin, adrenocorticotropin and cortisol secretion and disappearance in normal men

1993 ◽  
Vol 128 (6) ◽  
pp. 521-528 ◽  
Author(s):  
Ali Iranmanesh ◽  
German Lizarralde ◽  
Johannes D Veldhuis
Keyword(s):  
Plasma Concentrations ◽  
Metabolic Stress ◽  
Fold Increase ◽  
Volume Of Distribution ◽  
Mean Value ◽  
Cortisol Secretion ◽  
Daily Production ◽  
Deconvolution Analysis ◽  
The Mean ◽  
Normal Men

In the present study, we investigated the coordinate kinetic response of the corticotropic axis to the acute metabolic stress of hypoglycemia by applying deconvolution analysis to adrenocorticotropin (ACTH), β-endorphin and cortisol concentration-time series generated in seven normal men after intravenous administration of insulin. Hypoglycemic stress resulted in a 22-fold increase in the mean plasma concentration of ACTH to a maximum of 77±15 pmol/l, in conjunction with a 7.5-fold increase in the mean plasma β-endorphin concentration, the maximal value of which was 96±11 pmol/l. Plasma cortisol concentrations increased by 2.6-fold with a mean value of 734±14 nmol/l. Maximal plasma ACTH and β-endorphin concentrations were preceded by discrete secretory bursts with peak amplitudes of 10.5±2.7 and 10.6±2.0 pmol·I−1·min−1 (20-fold and ninefold increases compared to control), respectively. The mass of ACTH released was 114±20 pmol/l (3.4-fold increase), which corresponds to a total amount of 1.25 μg (50% of daily production and 0.5% of reported pituitary stores), assuming a distribution volume of 40 ml/kg. A total amount of 4.4±0.7 mg of cortisol was released after insulin-induced hypoglycemia, based on a mean cortisol secretory mass of 1088±137 nmol/l and a presumed 11.3-1 volume of distribution. Deconvolution-based estimates of the endogenous half-lives of ACTH, β-endorphin and cortisol were 17±0.6, 22±1.7 and 65±5.3 min, respectively. In summary, deconvolution analysis revealed a rapid coordinate activation of ACTH, β-endorphin and cortisol secretion after hypoglycemic stress, which correlated closely but temporally preceded increases in the respective plasma concentrations. Our inference that only a small fraction of pituitary ACTH content is released during hypoglycemic stress emphasizes the large reserve capability of the pituitary corticotropes. The percentage response of adrenal gland to the metabolic stress of hypoglycemia was of lesser magnitude, possibly owing to the rate-limiting properties of cortisol biosynthesis. We conclude that kinetic responses of the hypothalamic—pituitary—adrenal axis to hypoglycemic stress exhibit exquisite temporal synchrony and manifest a marked reserve capacity.

Inhibition by dexamethasone of arginine vasopressin and ACTH responses to insulin-induced hypoglycemia and cigarette smoking in normal men

1990 ◽  
Vol 123 (5) ◽  
pp. 487-492 ◽  
Author(s):  
P. Chiodera ◽  
V. Coiro
Keyword(s):  
Cigarette Smoking ◽  
Plasma Concentrations ◽  
Peak Level ◽  
Inhibitory Effect ◽  
Dexamethasone Treatment ◽  
Plasma Acth ◽  
The Mean ◽  
Normal Men ◽  
Circulating Levels ◽  
Acth Release

Abstract. Glucocorticoids are known to inhibit the AVP response to osmotic and hemodynamic stimuli in humans. In the present study, we examined whether the AVP response to other primary stimuli, such as insulin-induced hypoglycemia and cigarette smoking was sensitive to inhibition by dexamethasone. The plasma ACTH responses were also measured. Twenty-four normal men were randomly divided into 3 groups of 8 subjects. One group was tested with insulin (0.15 IU/kg in an iv bolus) and another group with cigarette smoking (2 non-filter cigarettes smoked in succession within 10 min) with and without pretreatment with dexamethasone (2 or 4 mg in an iv bolus 10 min before insulin or smoking). The third group was tested with dexamethasone alone (2 or 4 mg in an iv bolus). The administration of dexamethasone (2 or 4 mg) alone did not modify the circulating levels of AVP and ACTH at any time during the next hour. The hypoglycemic response to insulin was similar regardless of dexamethasone treatment. AVP rose sharply in response to both hypoglycemia and smoking, reaching mean peak levels at 45 and 30 min, respectively. After both stimuli, the mean peak levels of AVP were 2.25 times higher than baseline. Pretreatment with dexamethasone (2 or 4 mg) significantly decreased the AVP responses to both hypoglycemia and cigarette smoking. Following pretreatment with dexamethasone (2 or 4 mg) the AVP increments in response to hypoglycemia or cigarette smoking were only 1.7 times higher than baseline. The plasma concentrations of ACTH were strikingly increased by hypoglycemia. The mean peak level was 3.5 times higher than baseline and was reached at 45 min. Pretreatment with dexamethasone (2 or 4 mg) significantly reduced hypoglycemia-induced ACTH increase, with a mean peak response 2.8 times higher than baseline. Cigarette smoking significantly increased the plasma ACTH concentrations. The mean peak level was observed at 20 min and was 1.3 times higher than baseline. The ACTH response to smoking was not significant following pretreatment with dexamethasone (2 or 4 mg). These data show a partial inhibitory effect of dexamethasone on hypoglycemia-and cigarette smoking-stimulated AVP secretion. In addition, the data show suppression by dexamethasone of the ACTH response to cigarette smoking and confirm previous observations of a partial inhibition by glucocorticoids of hypoglycemia-induced ACTH release.

INFUSIONS OF hFSH AND hLH IN NORMAL MEN

1976 ◽  
Vol 81 (1) ◽  
pp. 234-242 ◽  
Author(s):  
J. M. Kjeld ◽  
S. F. Kuku ◽  
P. Harsoulis ◽  
T. R. Fraser ◽  
C. M. Puah ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Serum Testosterone ◽  
Significant Rise ◽  
Normal Male ◽  
Male Volunteers ◽  
Intravenous Infusions ◽  
Normal Men ◽  
Stimulating Hormone

ABSTRACT Standardized 4 h intravenous infusions of human follicle stimulating hormone (hFSH) and/or human luteinizing hormone (hLH) were given either separately or combined to 7 normal male volunteers. The infusions raised the serum gonadotrophin levels at least 10 (FSH) and 18 (LH) times above the basal ones. Serum testosterone (T) levels were measured serially before, during and after the infusions and, in 4 subjects, during a corresponding period of another normal day. During a normal or basal 24 h period fluctuations were seen and also a circadian rhythm with lower levels in the evening. The infusion of hFSH alone (3 subjects) did not alter the serum T levels. The infusion of hLH alone in 2 subjects raised serum T levels by 17% and 55% over those of the basal day. The combined FSH/LH infusion caused a significant rise (35–68%) in 4 subjects and greater rise in 2 of them than after infusion of the hLH alone. The serum T responses were gradual, reaching a maximum 7–8 h after the end of the infusion.

Adrenal and gonadal function in hypothyroid adult male rats

1997 ◽  
Vol 152 (1) ◽  
pp. 147-154 ◽  
Author(s):  
A Tohei ◽  
M Akai ◽  
T Tomabechi ◽  
M Mamada ◽  
K Taya
Keyword(s):  
Adult Male ◽  
Functional Relationship ◽  
Plasma Concentrations ◽  
Gonadal Hormones ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Male Rats ◽  
Plasma Acth ◽  
Corticosterone Release ◽  
Acth Release

Abstract The functional relationship between thyroid, adrenal and gonadal hormones was investigated using adult male rats. Hypothyroidism was produced by the administration of 4-methyl-2-thiouracil (thiouracil) in the drinking water for 2 weeks. Plasma concentrations of TSH dramatically increased, whereas plasma concentrations of tri-iodothyronine and thyroxine decreased in thiouracil-treated rats as compared with euthyroid rats. Hypothyroidism increased basal levels of plasma ACTH and pituitary content of ACTH. The pituitary responsiveness to CRH for ACTH release markedly increased, whereas the adrenal responsiveness to ACTH for corticosterone release decreased. These results indicated that hypothyroidism causes adrenal dysfunction in adult male rats. Pituitary contents of LH and prolactin decreased in hypothyroid rats as compared with euthyroid rats. In addition, hypothyroidism lowered pituitary LH responsiveness to LHRH. Testicular responsiveness to human chorionic gonadotrophin for testosterone release, however, was not different between euthyroid and hypothyroid animals. These results indicated that hypothyroidism causes adrenal dysfunction and results in hypersecretion of ACTH from the pituitary gland. Adrenal dysfunction may contribute to the inhibition of LHRH secretion from the hypothalamus, possibly mediated by excess CRH. Journal of Endocrinology (1997) 152, 147–154

Effects of the Glucocorticoid Antagonist RU 486 on Pituitary-Adrenal Function in Patients with Anorexia nervosa and Healthy Volunteers: Enhancement of Plasma ACTH and Cortisol Secretion in Underweight Patients

1993 ◽  
Vol 57 (6) ◽  
pp. 1082-1091 ◽  
Author(s):  
Mitchel A. Kling ◽  
Mark A. Demitrack ◽  
Harvey J. Whitfield, Jr. ◽  
Konstantine T. Kalogeras ◽  
Samuel J. Listwak ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Healthy Volunteers ◽  
Adrenal Function ◽  
Cortisol Secretion ◽  
Plasma Acth ◽  
Ru 486 ◽  
Underweight Patients

Premature birth of live lambs induced by pulsatile infusion of ACTH

1990 ◽  
Vol 124 (1) ◽  
pp. 99-107 ◽  
Author(s):  
R. J. MacIsaac ◽  
R. S. Carson ◽  
A. P. Horvath ◽  
E. M. Wintour
Keyword(s):  
Plasma Concentrations ◽  
Maternal Plasma ◽  
Sampling Time ◽  
Plasma Acth ◽  
Fetal Plasma ◽  
A Value ◽  
Normal Term ◽  
Acth Treatment ◽  
Normal Gestation ◽  
Pulsatile Infusion

ABSTRACT This study was designed to investigate the effects of pulsatile infusion of ACTH into ovine fetuses on the endocrine changes that precede parturition, the timing of birth and the subsequent survival of the lamb. Where appropriate, these parameters were compared with fetuses infused with pulses of saline and uninfused normal term fetuses. Ten fetuses received a 15-min infusion of synthetic ACTH(1–24) (79 ng/min) from day 125 (n=9) or day 126 (n=1) of gestation. Seven fetuses were born prematurely within 174±14 h (mean ± s.e.m.) after the commencement of the infusion, i.e. at 132 ± 0·6 days, whilst three died in utero at 130–131 days. When born all lambs could breath, walk and suckle. Of the seven premature lambs, four died 2–10 days after parturition but three survived for at least 12 months after birth. Fetuses infused with pulses of ACTH exhibited intermittent but very large increases in plasma ACTH values, with the first pulse, on day 1, increasing ACTH values from 5·1 ± 1·1 to 140 ± 31·3 pmol/l (P<0·001). At the next sampling time, ACTH values were not significantly different from preinfusion values. A similar plasma ACTH profile was observed on each subsequent day of ACTH treatment. In contrast, fetuses (n=4) infused with pulses of saline between 125 and 131 days exhibited fetal plasma concentrations of ACTH which ranged between 2 and 12 pmol/l for the majority of the time. Of the uninfused fetuses (n=8) that were studied during the last week of normal gestation, seven were born alive at 148·9± 1·0 days of gestation, whilst one lamb was stillborn at 146 days. In these fetuses, plasma concentrations of ACTH increased slowly to 35·6 ±2·4 pmol/l on the day before delivery with a further increase to 76·4± 3·9 pmol/l occurring on the day of delivery. In fetuses infused with pulses of ACTH there was also a significant (P< 0·001) increase in the fetal cortisol to corticosterone ratio from a value of 2·9 before the commencement of the infusion to 69·1 just before birth. In ewes bearing uninfused fetuses born at normal term, maternal plasma concentrations of progesterone on day 4 before delivery were significantly (P<0·05) lower than on day 5 before delivery. In comparison, in ewes bearing fetuses infused with pulses of ACTH, a significant (P<0·05) decrease from maternal plasma concentrations of progesterone on day 5 before delivery did not occur until day 1 before delivery. In ewes bearing uninfused or prematurely delivered fetuses infused with pulses of ACTH, maternal plasma concentrations of oestrogen did not significantly (P<0·01) increase until the day of parturition. It is concluded that a minimum of 6–7 days of ACTH treatment is required by the fetal adrenal for the induction of cortisol synthesis sufficient to produce the birth of viable lambs. However, premature lambs have a 57% mortality rate in the 2- to 10-day period after birth. Journal of Endocrinology (1990) 124, 99–107

Limitations to prediction of maximal oxygen intake

1964 ◽  
Vol 19 (5) ◽  
pp. 919-927 ◽  
Author(s):  
Loring B. Rowell ◽  
Henry L. Taylor ◽  
Yang Wang
Keyword(s):  
Metabolic Rate ◽  
Pulse Rate ◽  
Oxygen Intake ◽  
Physical Conditioning ◽  
Maximal Oxygen Intake ◽  
Before And After ◽  
Normal Men ◽  
Accuracy Of Prediction ◽  
Relationship Of ◽  
The Relationship

The predictability of maximal O2 intake (max Vo2) was studied in four groups of normal men, 18–24 years of age. Prediction of max Vo2 was made from pulse rate and Vo2 at a single submaximal workload at an ambient temperature of 78 F by use of the nomogram of Åstrand and Ryhming (1954) and underestimated actual max Vo2 by 27 ± 7% and 14 ± 7% in a sedentary group, before and after 2frac12–3 months of physical training, and by 5.6 ȁ 4% in a group of ten endurance athletes. Accuracy of prediction in all groups varied with approximation of pulse rate to 128 beats/min at 50% of max Vo2. Nonspecific stresses increased predictive errors in all groups. Constants b (slope) and A (intercept) in the regression equation Vo2 = bP – A (where P is pulse rate), were determined from Vo2 and pulse measured at four submaximal workloads requiring 13–28 ml O2/kg min. Prediction of max Vo2 by extrapolation of the slope to maximal pulse rate resulted in underestimation of 700–800 ml O2/min. Removal of 14% of circulating hemoglobin decreased max Vo2 by 4% but there was no change in pulse rates or predicted max Vo2. The relationship of RQ to V22 during work provided no reliable basis for prediction of max Vo2. exercise pulse rate, oxygen intake, relationship; pulse rate, oxygen intake relationship in exercise; metabolic rate, maximal aerobic prediction of; aerobic metabolic rate, maximal, prediction of; phlebotomy, effect on maximal oxygen intake, pulse rate; blood loss, effect on maximal oxygen intake, pulse rate; training, effect on maximal oxygen intake, pulse rates; physical conditioning, effect on maximal oxygen intake, pulse rates Submitted on October 4, 1963

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.

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