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ABSTRACT
The effect of stress on drinking, water balance and endocrine profile was studied using ten castrated rams. Individual sheep were exposed to 30-h periods of total isolation (psychological stress) or physical separation from their social group (control). Plasma was analysed for haematocrit, osmolality, electrolyte levels and concentrations of cortisol and arginine vasopressin. Isolation stress significantly reduced water intake, increased haematocrit and plasma concentration of cortisol, but did not alter osmolality or vasopressin concentration. The physiological effects of this self-imposed water restriction contrast with those obtained by depriving the sheep of water for 24 h under conditions that were not stressful, i.e. by keeping them grouped together. These results suggest that cortisol may act to defend plasma volume in sheep exposed to acute stress. The results also indicate that vasopressin probably should not be considered to be a 'stress hormone' in the sheep.
J. Endocr. (1987) 112, 305–310
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Laboratoire de Physiologie des Régulations, Faculté des Sciences Biologiques, Avenue du Général Ledere, 35031 Rennes Cedex, France
(Received 31 May 1977)
Reports of the response of the hypothalamo-hypophysial-adrenal axis to stress have involved measurement of the levels of corticosterone and/or adrenocorticotrophin (ACTH) in the plasma of intact and adrenalectomized rats. It is known that the size and kinetics of the adrenal response are dependent on the nature of the stress and the sex of the rat (Kitay, 1961; Lescoat, Jego, Beraud & Maniey, 1970). From work on the effect of stress on plasma ACTH (Lutz, Koch & Miahle, 1969; Cook, Kendall, Greer, & Kramer 1973; Usategui, Oliver, Vaudry, Lombardi, Rosenberg & Mourre, 1976), the nature of the stress and the parameters of the response appear to be related and Barrett (1960) reported that the release of ACTH in response to stress is greater in female than in male rats. This
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ABSTRACT
In-situ hybridization histochemistry was used to measure corticotrophin-releasing factor mRNA and proenkephalin A mRNA in the paraventricular nucleus (PVN), and pro-opiomelanocortin (POMC) mRNA in the anterior pituitary of the rat. Levels of message were determined at 1, 2, 4 and 8 h after exposure to a variety of physical and psychological stresses. Corticotrophin-releasing factor mRNA in the PVN and POMC mRNA in the anterior pituitary increased in response to i.p. hypertonic saline, restraint and swim stress but not to cold stress. Proenkephalin A mRNA was raised only in response to the physical stress of i.p. injection of hypertonic saline. These results suggest that different afferent pathways and hypothalamic neurotransmitters may be involved in mediating the hypothalamic response to different physical and psychological stresses.
Journal of Endocrinology (1989) 122, 705–711
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ABSTRACT
Melanin-concentrating hormone (MCH) is a neurohypophysial peptide that induces pigmentary pallor in teleosts and which is released when the fish are placed on a white background. An additional effect of the peptide is the depression of ACTH and hence cortisol secretion during moderate stress. The present work on rainbow trout shows that plasma MCH concentrations, while unaffected by a single stress, are raised by repeated stress (1 ml saline injected i.p. without anaesthesia) and remain high for several hours thereafter. The response to stress is observed only in white-adapted fish and not in fish kept in black-coloured tanks, when MCH release is normally low. Plasma concentrations of MCH vary diurnally but stress induces an equivalent incremental rise in plasma MCH, whether administered in the middle or towards the end of the photophase. The stress-induced rise in MCH concentrations is prevented by treatment with dexamethasone. The results support the suggestion that the modulatory effect of MCH on the hypothalamopituitary-interrenal axis of fish might be enhanced under conditions of stress.
Journal of Endocrinology (1991) 128, 261–266
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ABSTRACT
A hypothalamic site of action has been hypothesized for the inhibitory effect of chronic stress on gonadotrophin secretion. The aim of the present study was to examine the temporal changes in hypothalamic LHRH content and gonadotrophin secretion during restraint stress, and the pituitary responsiveness to LHRH stimulation in chronically stressed rats. Adult male rats were killed after being restrained for 0, 20, 45, 90, 180 and 360 min or for 6 h daily over 2, 3 and 4 days. After 20–45 min of stress there was an increase in plasma concentrations of LH (P<0·01) and a decrease in hypothalamic LHRH content (P<0·01), suggesting a negative correlation between plasma LH and hypothalamic LHRH concentrations. Plasma concentrations of FSH were also increased by restraint, but the FSH response was slower and less than the plasma LH response, being significant after 90 min of restraint. Plasma LH and FSH and hypothalamic LHRH concentrations were decreased in chronically stressed rats. In rats restrained for 6 h daily over 4 days, the response of plasma gonadotrophins to administration of 500 ng LHRH was enhanced 45 min after the injection. On the basis of these observations we concluded that in the intact rat, stress may acutely stimulate LHRH and gonadotrophin secretion, and the inhibitory effect of chronic stress on plasma LH and FSH seems not to be due to a reduction in pituitary responsiveness to LHRH, but rather to a decrease in LHRH secretion.
Journal of Endocrinology (1990) 124, 241–246
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Plasma cortisol is largely bound to corticosteroid-binding globulin (CBG), which regulates its bioavailability by restricting exit from capillaries. Levels of CBG may be altered by several factors including stress and this can influence the amount of cortisol reaching cells. This study investigated the effect of social instability on plasma concentrations of CBG, total and free (not protein bound) cortisol in horses. Horses new to our research herd ('newcomers') were confined in a small yard with four dominant resident horses for 3-4 h daily for 3-4 (n = 5) or 9-14 (n = 3) days. Jugular blood was collected in the mornings from newcomers before the period of stress began ('pre-stress'), and then before each day's stress. Residents were bled before stress on the first and thirteenth day. Residents always behaved aggressively towards newcomers. By the end of the stress period, all newcomers were subordinate to residents. In newcomers (n = 8) after 3-4 days of social stress, CBG binding capacity had fallen (P = 0.0025), while free cortisol concentrations had risen (P = 0.0016) from pre-stress values. In contrast, total cortisol did not change. In residents, CBG had decreased slightly but significantly (P = 0.0162) after 12 days of stress. Residents and newcomers did not differ in pre-stress CBG binding capacity, total or free cortisol concentrations. However, by the second week of stress, CBG binding capacity was lower (P = 0.015) and free cortisol higher (P = 0.030) in newcomers (n = 3) than in residents. Total cortisol did not differ between the groups. In conclusion social stress clearly affected the adrenal axis of subordinate newcomer horses, lowering the binding capacity of CBG and raising free cortisol concentrations. However, no effect of stress could be detected when only total cortisol was measured. Therefore, to assess adrenal axis status accurately in horses, it is essential to monitor the binding capacity of CBG and free cortisol concentrations in addition to total cortisol levels.
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SUMMARY
Six groups each of 12 male albino rats were reared from day 21 of life at temperatures of 23, 34 or 37 °C. While the rats survived for unlimited periods at 23 and 34 °C, the animals reared at 37 °C succumbed within 5 days to heat stress. The latter group, when injected s.c. or i.p. with 50 mg dehydroepiandrosterone (DHA)/kg/day were no longer affected by the heat. During this treatment thyroid epithelial cell height doubled, colloid decreased by 20%, connective tissue did not change, the basic metabolic rate decreased by 10% and rectal temperatures of the treated rats increased with the ambient temperatures. Body weight increased only slightly, pituitary TSH decreased by 25%, serum TSH increased by over 50%, thyroxine and 125I uptake increased by 200%. The survival of the DHA-treated rats was apparently secured by blocking the hypothalamic thermoreceptors.
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ABSTRACT
We have previously found that modifications to serum progesterone concentration have profound inhibitory effects on prolactin release in response to ether stress. The objective of the present study was to determine the effect of ether stress on progesterone secretion and the role of this steroid in ether-induced prolactin release.
Serum progesterone concentration, 5 min after ether stress had been applied over a 2-min period, was consistently increased in male rats, in cyclic rats on the mornings of pro-oestrus and oestrus, and in androgenized rats in permanent oestrus. Ovariectomized androgenized rats showed the same response. Adrenalectomy of male and female rats abolished the progesterone increase induced by stress. Thus, the progesterone secreted by stressed rats is mostly of adrenal origin.
In groups of male and pro-oestrous rats, circulating concentrations of prolactin and progesterone were measured from 5 to 60 min after stress. In both sexes the serum prolactin concentration was significantly increased at only 5 and 10 min after stress when compared with control values. In pro-oestrous rats the serum progesterone concentration was significantly higher than in controls at 5, 10 and 20 min after stress, whilst in male rats the concentration remained significantly higher at 30 min.
Thirty minutes after the first stress, male and pro-oestrous rats were etherized for 2 min, and bled 5 min after removal from the ether container. In female rats this second stress produced only a slight but significant increase in serum prolactin concentrations, whereas in male rats prolactin concentrations did not increase. The second stress was still capable of significantly increasing circulating progesterone concentrations to levels similar to those obtained after the first stress in animals from all groups. Thus, an increased circulating progesterone concentration did not lead to regulation of further progesterone secretion. To find whether this type of response was due to a blocking effect of the previously released progesterone, animals were injected with the anti-progesterone RU 38486 (17β-hydroxy-11β-(4-dimethylaminophenyl)-17α-propinyl-oestra-4,9-dien-3-one) or with a specific antibody raised against progesterone. In both groups of treated rats the second stress induced a significant increase in serum prolactin and progesterone concentrations to give values similar to those obtained after the first stress. When the second stress was applied to female rats 60 min after the first the prolactin response was comparable to that obtained after the first exposure to ether.
In conclusion, we have demonstrated that serum prolactin and progesterone concentrations are significantly increased after ether stress, and that the latter hormone exerts an inhibitory regulatory feedback on prolactin secretion. These results provide an important new insight into the role of progesterone in the regulation of prolactin release.
Journal of Endocrinology (1989) 120, 37–43
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Diabetes and Obesity Research Program, Department of Medicine, Garvan Institute of Medical Research, St Vincent's Hospital, 384 Victoria Street, Darlinghurst, Sydney 2010, New South Wales, Australia
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stress signalling pathways that have recently been suggested to be mediators of the insulin resistance seen in diabetes and obesity. Specifically, it has been postulated that excess FA can activate the c-Jun N-terminal kinase (JNK; Hirosumi et al . 2002
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SUMMARY
Cortisol pools were examined in six shorn sheep before (i.e. control conditions) and during their exposure to a cold, wet environment. Cortisol labelled with tritium was infused until equilibrium concentration [3H(eq)] was reached in the plasma; the infusion was then stopped and the instantaneous concentrations [3H(t)] determined at intervals during the next 20–40 min. A two-pool model was used to calculate results and the rate constants k 10, k 12 and k 21 were used to describe catabolism of hormone from the central pool, movement from the central to the outer pool and in the reverse direction respectively.
In the majority of cases when the fractional concentrations, [3H(t)]/-[3H(eq)], after infusion were plotted against time, curves representing control conditions indicated that the apparent rate of disappearance of cortisol from plasma was faster than from cold-stressed normothermic sheep. The apparent rate of disappearance of cortisol from the plasma of both control and cold-stressed normothermic sheep was faster than when the animals were hypothermic. These results were not obtained in two sheep when they were cold-stressed and normothermic and these are discussed.
The rate constants k 10, k 12 and k 21 obtained in the experiments bore the relation control < cold-stressed normothermic < hypothermic. The total amount of cortisol increased about 4 times, relative to control, when the sheep were cold-stressed and normothermic, and 40 times, relative to control, when they were hypothermic. Pools decreased in one cold-stressed normothermic sheep. Turnover rates were 7·7%, 7·0% and 3·7% of the total pool/min for sheep under control, cold-stressed normothermic and hypothermic conditions respectively.
It is concluded that the greatly increased plasma cortisol concentrations detected in cold-stressed normothermic and hypothermic sheep were associated with great increases in total cortisol, distributed in relatively constant 'spaces' in the body under those conditions.
