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Cortisol metabolism was studied in conscious adult male guinea-pigs subjected to a neurotrophic stress (immobilization and stimulation by light for 3 h).
The disappearance curves of tracer quantities of [3H]cortisol were represented by a two-pool model. In stressed animals, there was a marked increase in the mean plasma level of cortisol (184% of control value; P <0·001) and in the metabolic clearance rate (MCR; 17% of control value; 0·001 <P <0·01). This rise in the MCR of plasma cortisol resulted from an increase in the mean total apparent volume of distribution (49%, P < 0·001). The lack of significant differences in the slopes of the second exponential phase of the disappearance curves indicated that the stress did not significantly increase the half-life of cortisol. The mean binding capacity of transcortin for cortisol (ST) was significantly higher in the animals which had been subjected to the neurotrophic stress than in the control guinea-pigs (0·02 < P <0·05). However, ST values remained very low and accounted for the very high levels of free cortisol found after the stress. The results suggest that the raised concentrations of unbound cortisol found in the plasma of conscious adult male guinea-pigs in response to neurotrophic stress reflect a hypersecretion of corticosteroid.
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SUMMARY
The uptake of 131I by the thyroid of the rat has been investigated under various conditions of stress.
The acute change always consists in a considerable reduction of the rate of uptake of 131I irrespective of the nature of the stress.
This acute inhibition in the uptake of 131I is independent of the anterior pituitary lobe, since it occurs in the normal and hypophysectomized animal alike. It is also independent of the presence of the adrenals. The inhibition of the uptake of 131I by the thyroids occurs in vivo only; their ability to take up 131I in vitro is not impaired.
All the acute changes seen under stress conditions can be readily reproduced by treatment with adrenaline, which shows the same inhibitory effect on normal and hypophysectomized animals, the action being equally transitory.
It is suggested that the acute changes in thyroid function seen under stress conditions are entirely independent of the anterior pituitary and are caused by increased release of vasoconstrictor substances.
An increased uptake rate of 131I by the thyroid was seen 24 hr after the acute stress. This was thought to be caused by a compensatory increase in the secretion of thyrotrophic hormone by the anterior pituitary.
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SUMMARY
Changes in pituitary and plasma corticotrophin (ACTH), estimated by redox bioassay, were correlated with changes in plasma corticosterone in adrenalectomized rats, with and without corticosterone treatment, before and after exposure to stress. After adrenalectomy, the plasma ACTH concentration was persistently increased. The pituitary ACTH content declined and then increased markedly. These changes were prevented by physiological doses of corticosteroids. Stress caused only a small rise in the plasma ACTH concentration in intact and sham-operated rats but a marked increase in adrenalectomized animals. This exaggerated response was reduced to normal by physiological doses of corticosterone. Prolonged treatment with higher doses of corticosterone was necessary to abolish completely the adrenocorticotrophic response to stress. However, one injection of the steroid, in a dose sufficient to raise the plasma corticosterone concentration to a similar level, did not impair the stress-induced release of ACTH. The results suggest that the synthesis and the basal release of ACTH are directly controlled by the concentration of corticosteroid in the blood, but the corticosteroids exert only a delayed effect in modulating the stress-induced release of the hormone.
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ABSTRACT
We examined the effects of acute stress on the immune system and disease resistance of juvenile chinook salmon (Oncorhynchus tshawytscha) in laboratory and clinical trials. Immune function, as measured by the ability of lymphocytes from the anterior kidney to generate specific antibody-producing cells (APC) in vitro, was depressed 4 h after stress, when plasma cortisol levels were highest. At the same time, resistance to the fish pathogen, Vibrio anguillarum, was also depressed. Compared with controls, plasma cortisol and APC of stressed fish were unchanged after 24 h, and disease resistance was enhanced as evidenced by higher survival rate and longer mean time to death of mortalities. After 7 days, even though numbers of APC were depressed, plasma cortisol concentration and disease resistance did not differ from controls. This pattern was generally the same, independent of the type of stress applied: i.e. being held out of water in a dipnet for 30 s, manipulation during hatchery operations for 4 h, or transportation for 9 h. These and earlier findings suggest that similar endocrine-immune interactions operate in the mammalian and salmonid systems during acute stress.
Journal of Endocrinology (1989) 120, 135–142
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SUMMARY
Partial and complete deafferentation of the hypothalamus of the pigeon was performed using a modified Halasz-Pupp microknife. After complete neural isolation the plasma corticosterone level stabilized at a point intermediate between the morning and evening levels found in intact pigeons. No diurnal rhythm was observed and the response to neurogenic stimulus (restraint) was suppressed. Ether stress, however, induced a rise in plasma corticosterone. Posterior deafferentation had no effect on the diurnal corticosterone rhythm but did block the rise normally found after restraint. Anterior deafferentation did not suppress the stress-induced response but provided the cuts were large enough they inhibited the diurnal corticosterone rhythm.
It is suggested therefore that the neural afferents to the hypothalamus which are necessary for diurnal fluctuations in pituitary-adrenal function pass through a sector located anteriorly between 45° and 60° on either side of the mid-line while stress-induced adrenocortical activation is triggered through posterior connexions.
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Successful existence depends on the ability to cope with an immense variety of complex challenges or stressors and to mount an 'appropriate' response to any particular situation. While the concept of stress is readily understood, a definition acceptable to more than a handful of individuals remains elusive. It is necessary therefore at the outset to clarify the context within which we have written the current review. We will utilize a simple definition based on the neuroendocrine response to stressors and for this purpose we shall limit our discussion to those events resulting in the activation of the hypothalamo-pituitary-adrenal (HPA) axis. The final stage of this activation is the secretion of glucocorticoids from the adrenal cortex.
Glucocorticoids have a wide range of actions affecting many aspects of bodily function including metabolism, inflammation and immunity. Glucocorticoids also control their own synthesis and release by completing a negative feedback loop at the level
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ABSTRACT
When maternal stress, containing a large anxiety component, was administered during pregnancy there was a significant decrease in 3β-hydroxysteroid dehydrogenase (3β-HSD) activity in the fetal testis from days 16 to 20 of gestation, but not at birth nor in the first week after birth. However, persistent effects were found in adult males of 90 days of age. Basal testosterone concentrations in both plasma and testes and testicular 3β-HSD activity were significantly lower whilst basal plasma progesterone concentrations were significantly higher in the stressed group. When the stressed offspring were subjected to short-term stress (one session), their plasma testosterone concentration was significantly below that of the controls. It is suggested that suppressed gonadotrophin secretion during critical periods of development alters fetal testicular function, and that raised circulating levels of stress-induced hormones such as β-endorphin may be responsible for changes in gonadotrophin secretion.
J. Endocr. (1985) 107, 241–245
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There is growing evidence that prenatal adversities could be implicated in foetal programming of adult chronic diseases. Since maternal stress is known to disturb the foetal glucocorticoid environment, we examined the consequences of prenatal stress on foetal growth, on glucose-insulin metabolism and on feeding behaviour in the aged male rat. In foetuses at term, maternal stress reduced body, adrenal and pancreas weight as well as plasma corticosterone and glucose levels. In aged male rats (24 months of age), prenatal stress induced hyperglycaemia and glucose intolerance and decreased basal leptin levels. Moreover, after a fasting period, they showed an increased food intake. These data suggest that maternal stress induces a long-lasting disturbance in feeding behaviour and dysfunctions related to type 2 diabetes mellitus. This programming could be linked to the early restricted foetal growth and to the adverse glucocorticoid environment in utero.
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-fat-induced insulin resistance is not clear. Recently, we ( Vinayagamoorthi et al . 2006 ) along with others ( Rudich et al . 1997 , 1999 , Maddux et al . 2001 ) reported the role of oxidative stress in the pathogenesis of insulin resistance. A decline in reduced
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ABSTRACT
The effects of restraint stress and opiates on prolactin secretion in male rats have been measured. Both induced a short-lived increase in prolactinaemia. Experimental evidence indicates that both opioids and restraint stress bring about their actions by the activation of opioid receptors. When restraint stress was followed by administration of the specific κ-agonist bremazocine, a second prolactin peak was observed. In contrast, morphine (predominantly a μ-agonist) lost its prolactin-stimulating capacity when given after a period of restraint stress. This indicates cross-tolerance between restraint stress and morphine. Tolerance was overcome when the dose of morphine was doubled, and an increase in prolactin secretion could again be obtained. The cross-tolerance phenomenon argues that a common opioid receptor is involved in morphine- and restraint stress-stimulated prolactin release. In another set of experiments, in which morphine administration replaced restraint stress as a means of inducing tolerance, a second rise in prolactinaemia was seen only with bremazocine and not with a further administration of morphine. This suggests a morphine (μ) receptor-specific development of tolerance. Two consecutive administrations of bremazocine also produced tolerance, in this case for the κ-receptor. This illustrates the rapid and receptor-specific development of tolerance for the prolactin-releasing capacity of opioid compounds.
Journal of Endocrinology (1991) 128, 281–285
