RELATIONSHIP BETWEEN INCREASES IN PLASMA CORTISOL CONCENTRATION AND RATE OF CORTISOL SECRETION DURING EXERCISE IN MAN

1977 ◽  
Vol 72 (1) ◽  
pp. 109-110 ◽  
Author(s):  
G. C. CASHMORE ◽  
C. T. M. DAVIES ◽  
J. D. FEW
1974 ◽  
Vol 62 (2) ◽  
pp. 371-383 ◽  
Author(s):  
J. Y. F. PATERSON ◽  
J. L. LINZELL

SUMMARY Glucose entry rate was measured by primed infusion of [2-3H]glucose, and cortisol secretion rate by infusion of [1,2-3H2]cortisol, in two cows from 142 days before calving to day 287 of lactation. Mammary blood flow and the mammary uptake of glucose and cortisol were also measured. In late pregnancy, cortisol secretion rate was 8·6 ± 3·17 (s.d.) μg/min and plasma cortisol concentration was 1·8 ± 0·52 μg/l. During parturition in one animal the secretion rate was 92 μg/min and plasma cortisol concentration was 15 μg/l. During lactation the secretion rate (26·4 ± 7·14 μg/min) and plasma cortisol concentration (5·6 ± 0·73 μg/l) were significantly greater than in dry cows. The mammary uptake of cortisol was 3 to 4% of the secretion rate in both dry and lactating cows. Glucose entry rate was 5·77 ± 2·250 (s.d.) mg/min/kg0·75 in dry cows and there was no significant mammary uptake of glucose. During lactation the glucose entry increased to 9·45 ± 1·881 mg/min/kg0·75. Mammary uptake of glucose was 3·56 ± 1·949 mg/min/kg0·75. The non-mammary utilization of glucose, glucose entry less mammary uptake, was the same for dry and lactating cows. There was a good correlation between glucose entry and milk yield, and between mammary uptake of glucose and milk yield. Since the mammary arterio-venous glucose concentration difference was relatively constant, it is suggested that the change in mammary blood flow may determine the change in glucose uptake and milk yield.


1985 ◽  
Vol 110 (4) ◽  
pp. 546-552 ◽  
Author(s):  
E. Domański ◽  
E. Stupnicka ◽  
F. Przekop ◽  
E. Wolińska-Witort

Abstract. It has previously been observed that sheep subjected to repeated and prolonged stress stimuli showed biphasic cortisol responses. On the first and second day of stimulation an elevation was observed, while on the subsequent days and on the day after the stimulation a marked suppression of plasma cortisol level and a disappearance of its circadian rhythm was noted. It was hypothesized that these changes in the secretion of the hormone were caused by the alteration of catecholaminergic systems in the CNS. To verify this suggestion chemical lesions of the catecholergic systems of the diencephalon were carried out by the infusion of 6-hydroxydopamine (6-OHDA) into the third cerebral ventricle and animals treated in this fashion were subjected to repeated and prolonged electrical mild footshocking (applied during 3 days). The pretreated animals lost the circadian rhythm in cortisol secretion on the days before as well as during and after the electrical stimulation. The animals pretreated with 6-OHDA showed a significant rise of the plasma cortisol level during stimulation. This rise, as the highest daily concentration, occurring within about 1 h after the beginning of footshocking, was significantly accelerated in time with respect to the physiological acrophase, occurring in the early morning hours at the end of prestimulatory days. On the other hand, the pretreated animals did not show the decrease of plasma cortisol levels on the day after the stimulation, observed in normal non-pretreated ones. It is suggested that the absence of the suppression of plasma cortisol concentration in the animals pretreated with 6-OHDA on the day after the stimulation may be due to the blockade of the ventral noradrenergic bundle innervating the medial basal hypothalamus, while disappearance of the circadian rhythm of cortisol secretion was due to the disturbance in the function of retinohypothalamic projection.


1972 ◽  
Vol 55 (2) ◽  
pp. 335-350 ◽  
Author(s):  
J. Y. F. PATERSON ◽  
F. A. HARRISON

SUMMARY The uptake of cortisol by the gastro-intestinal tract and by the liver was estimated in sheep by measurement of [3H]cortisol concentrations in portal and hepatic venous plasma during constant infusion of tritium-labelled cortisol, with simultaneous measurement of plasma flows. The total splanchnic uptake of cortisol was 57 ± 4 (s.e.m.)% of the measured rate of cortisol secretion, 45% by the liver and the remainder by the gastro-intestinal tract. The splanchnic extraction of cortisol could be related to plasma flow, and was less efficient at higher flows. It could also be related to plasma cortisol concentration, and was more efficient at higher concentrations. The splanchnic uptake of cortisol was closely correlated with the flow of unbound cortisol into the region, and was 1·61 times that influx. There is therefore partial dissociation of plasma protein-bound cortisol during the splanchnic uptake. About 25% of secreted cortisol is converted to cortisone at extrahepatic sites, and is removed from plasma by the liver.


2018 ◽  
Vol 18 (1) ◽  
pp. 185-193
Author(s):  
Witold Kędzierski ◽  
Zbigniew Bełkot

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.


2012 ◽  
Vol 303 (10) ◽  
pp. E1190-E1201 ◽  
Author(s):  
David Thorsley ◽  
Rachel Leproult ◽  
Karine Spiegel ◽  
Jaques Reifman

Both circadian rhythmicity and sleep play significant roles in the regulation of plasma cortisol concentration by the hypothalamo-pituitary-adrenal (HPA) axis. Numerous studies have found links between sleep and changes in cortisol concentration, but the implications of these results have remained largely qualitative. In this article, we present a quantitative phenomenological model to describe the effects of different sleep durations on cortisol concentration. We constructed the proposed model by incorporating the circadian and sleep allostatic effects on cortisol concentration, the pulsatile nature of cortisol secretion, and cortisol's negative autoregulation of its own production and validated its performance on three study groups that experienced four distinct sleep durations. The model captured many disparate effects of sleep on cortisol dynamics, such as the inhibition of cortisol secretion after the wake-to-sleep transition and the rapid rise of cortisol concentration before morning awakening. Notably, the model reconciled the seemingly contradictory findings between studies that report an increase in cortisol concentration following total sleep deprivation and studies that report no change in concentration. This work provides a biomathematical approach to combine the results on the effects of sleep on cortisol concentration into a unified framework and predict the impact of varying sleep durations on the cortisol profile.


2010 ◽  
Vol 298 (4) ◽  
pp. L575-L583 ◽  
Author(s):  
Sandra Orgeig ◽  
Tamara A. Crittenden ◽  
Ceilidh Marchant ◽  
I. Caroline McMillen ◽  
Janna L. Morrison

Pulmonary surfactant is synthesized by type II alveolar epithelial cells to regulate the surface tension at the air-liquid interface of the air-breathing lung. Developmental maturation of the surfactant system is controlled by many factors including oxygen, glucose, catecholamines, and cortisol. The intrauterine growth-restricted (IUGR) fetus is hypoxemic and hypoglycemic, with elevated plasma catecholamine and cortisol concentrations. The impact of IUGR on surfactant maturation is unclear. Here we investigate the expression of surfactant protein (SP) A, B, and C in lung tissue of fetal sheep at 133 and 141 days of gestation (term 150 ± 3 days) from control and carunclectomized Merino ewes. Placentally restricted (PR) fetuses had a body weight <2 SD from the mean of control fetuses and a mean gestational PaO2<17 mmHg. PR fetuses had reduced absolute, but not relative, lung weight, decreased plasma glucose concentration, and increased plasma cortisol concentration. Lung SP-A, -B, and -C protein and mRNA expression was reduced in PR compared with control fetuses at both ages. SP-B and -C but not SP-A mRNA expression and SP-A but not SP-B or -C protein expression increased with gestational age. Mean gestational PaO2was positively correlated with SP-A, -B, and -C protein and SP-B and -C mRNA expression in the younger cohort. SP-A and -B gene expression was inversely related to plasma cortisol concentration. Placental restriction, leading to chronic hypoxemia and hypercortisolemia in the carunclectomy model, results in significant inhibition of surfactant maturation. These data suggest that IUGR fetuses are at significant risk of lung complications, especially if born prematurely.


1960 ◽  
Vol 21 (2) ◽  
pp. 171-176 ◽  
Author(s):  
S. SHUSTER

SUMMARY Plasma cortisol concentrations increased after injections of nicotine. This increase was variable and was no greater than that seen after substitution of normal saline for nicotine. Plasma cortisol concentrations did not increase after nicotine in patients with hypopituitarism and after inhibition of corticotrophin release with triamcinolone. It is concluded that the increased plasma cortisol concentration after injection of nicotine was due to non-specific pituitary stimulation associated with the experimental procedure and not due to any direct effect of the nicotine. Nicotine resulted in a similar increase in plasma cortisol in four patients with diabetes insipidus. Neither rapid infusion of hypertonic mannitol nor ingestion of ethanol had a consistent effect on the plasma cortisol concentration. It is therefore concluded that the antidiuretic hormone is not the 'corticotrophin release factor' in man.


1980 ◽  
Vol 8 (5) ◽  
pp. 587-588 ◽  
Author(s):  
JUDITH M. BAKER ◽  
SHEILA L. HANDLEY ◽  
GILL WALDRON ◽  
T. LESLIE DUNN

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