Dissociation of adrenal corticosteroid production from ACTH in water-restricted female rats

1981 ◽  
Vol 241 (1) ◽  
pp. R21-R24 ◽  
Author(s):  
R. G. Doell ◽  
M. F. Dallman ◽  
R. B. Clayton ◽  
G. D. Gray ◽  
S. Levine
Keyword(s):  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Female Rats ◽  
Adrenocorticotrophic Hormone ◽  
Corticosterone Concentration ◽  
Acth Concentration

These experiments were undertaken to investigate the mechanism whereby a precipitous drop in plasma corticosterone concentration is brought about following drinking in rats on a restricted water schedule. No alteration in adrenocorticotrophic hormone (ACTH) output was found, nor was catabolism of corticosterone sufficient to account for the drop. It is concluded that corticosterone level is controlled under these conditions by a mechanism independent of ACTH concentration.

INTERRELATIONSHIPS OF PITUITARY AND PLASMA CORTICOTROPHIN AND PLASMA CORTICOSTERONE IN ADRENALECTOMIZED AND STRESSED, ADRENALECTOMIZED RATS

1974 ◽  
Vol 63 (1) ◽  
pp. 213-222 ◽  
Author(s):  
JULIA C. BUCKINGHAM ◽  
J. R. HODGES
Keyword(s):  
Plasma Corticosterone ◽  
Prolonged Treatment ◽  
Delayed Effect ◽  
Plasma Acth ◽  
Corticosterone Concentration ◽  
Before And After ◽  
Small Rise ◽  
Acth Concentration ◽  
Corticosterone Treatment ◽  
Adrenalectomized Rats

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.

Hypothalamus and endocrine function in persistent estrous rats at low environmental temperature

1960 ◽  
Vol 199 (4) ◽  
pp. 701-706 ◽  
Author(s):  
Savino A. D'Angelo
Keyword(s):  
Ascorbic Acid ◽  
Acid Concentration ◽  
Ovarian Function ◽  
Hormone Secretion ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Female Rats ◽  
Endocrine Function ◽  
Ascorbic Acid Concentration ◽  
Hypothalamic Lesions

Persistent vaginal estrus with uterine and pituitary hypertrophy were found in adult female rats 4–10 months after placement of preoptic and anterior hypothalamic lesions. Serum TSH, I131 release rate and histology of the thyroid and ascorbic acid concentration of adenohypophysis, ovary and adrenal were normal. Exposure of lesioned rats to cold (5°C, 36–55 days) profoundly altered pituitary-target gland functions. Ovarian atrophy and uterine involution resulted; vaginal cornification ceased. Pituitary hypertrophy was inhibited but ascorbic acid concentration was maintained. Serum and pituitary TSH levels decreased and acceleration of thyroidal radioiodine release was prevented. Apparent dichotomy in adrenal responses developed. Despite enlarged adrenals, plasma corticosterone level in cold stressed, operated rats averaged less than one-third that of intact controls. Adrenal ascorbic acid concentration remained normal. The results underscore the basic role of central nervous mechanisms in endocrine function under chronic cold stress. Hypothalamic lesions which permit adequate trophic hormone secretion at normal temperatures drastically curtail thyroidal and ovarian function and selectively limit adrenal responses in the cold.

Effect of adenosine analogues on plasma corticosterone concentration in rats

1992 ◽  
Vol 127 (5) ◽  
pp. 471-475 ◽  
Author(s):  
Edmund Przegaliński ◽  
Bogusława Budziszewska ◽  
Anna Grochmal
Keyword(s):  
Adenosine Receptor ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Receptor Antagonists ◽  
Corticosterone Concentration ◽  
Adenosine Analogues ◽  
Negative Results ◽  
Corticosterone Secretion ◽  
Corticosterone Response ◽  
Pharmacological Blockade

In this study we examined the effect of the adenosine analogues: N6-cyclohexyladenosine, L-N6-phenylisopropyladenosine and 5′-N-ethylcarboxamidoadenosine on the plasma corticosterone concentration in rats. It was found that N6-cyclohexyladenosine (0.1–3.0 mg/kg), L-N6-phenylisopropyladenosine (0.1–1.0 mg/kg) and 5′-N-ethylcarboxamidoadenosine (0.01–1.0 mg/kg) dose-dependently increased the plasma corticosterone level. The effects of N6-cyclohexyladenosine (0.1 mg/kg) and L-N6-phenylisopropyladenosine (0.1 mg/kg) were completely blocked in animals pretreated with dexamethasone (3 × 1 mg/kg), as well as in animals with a pharmacological blockade of the release of hypothalamic corticotropin-releasing factor induced by chloropromazine (10 mg/kg), morphine (20 mg/kg) and nembutal (25 mg/kg), whereas the corticosterone response to 5′-N-ethylcarboxamidoadenosine (0.01 mg/kg) was blocked in dexamethasone-pretreated rats only. On the other hand, the adenosine receptor antagonists: 8-(p-sulfophenyl)-theophylline (30 mg/kg), 8-phenyltheophylline (10 and 30mg/kg), 1,3-dipropyl-8-(2-amino-4-chloro)-phenylxanthine (1 and 3 mg/kg) and 1,3-dipropyl-7-methylxanthine (1 mg/kg) did not affect the corticosterone response to N6-cyclohexyladenosine, L-N6-phenylisopropyladenosine or 5′-N-ethylcarboxamidoadenosine. The obtained results indicate that N6-cyclohexyladenosine and L-N6-phenylisopropyladenosine stimulate the corticosterone secretion at the hypothalamic level, whereas 5′-N-ethylcarboxamidoadenosine is likely to act at the pituitary level. Although the effects produced by the adenosine analogues show that both A1 and A2 receptors are involved in the corticosterone response, negative results of the interaction studies with adenosine receptor antagonists indicate that further experiments are necessary to elucidate this problem.

Relationship among sensitivity to adrenaline, plasma corticosterone level; and estrous cycle in rats

1995 ◽  
Vol 73 (5) ◽  
pp. 602-607 ◽  
Author(s):  
M. L. V. Rodrigues ◽  
F. K. Marcondes ◽  
R. C. Spadari-Bratfisch
Keyword(s):  
Estrous Cycle ◽  
Dose Response ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Female Rats ◽  
Extraneuronal Uptake ◽  
Response Curves ◽  
Experimental Conditions ◽  
Dose Response Curves ◽  
Right Atria

The dose–response curves to the chronotropic effect of adrenaline obtained in right atria isolated from female rats indicated an order of increasing sensitivity to adrenaline, at the pD2 level, according to the estrous cycle, as follows: estrus ≤ metestrus ≤ diestrus ≤ proestrus. Inhibition of neuronal and extraneuronal uptake shifted the dose–response curves to adrenaline to the left only in right atria isolated from rats during estrus or metestrus. Moreover, under these experimental conditions, right atria were subsensitive to adrenaline during proestrus, in contrast to metestrus. Plasma corticosterone levels were lower during estrus and higher at proestrus. There was a positive correlation between right atria sensitivity to adrenaline and plasma corticosterone levels and estrous cycle phases. Our results also suggest that in the rat right atria during proestrus, as opposed to the other phases of the estrous cycle, there was an endogenous inhibition of extraneuronal uptake together with some alteration at the adrenoceptor level and (or) at intracellular mechanisms beyond receptors.Key words: adrenergic response, female, adrenaline, chronotropism, right atria.

The hypophyseal–adrenocortical response to various different stressing procedures in ACTH-treated rats

1968 ◽  
Vol 46 (4) ◽  
pp. 567-571 ◽  
Author(s):  
E. Stark ◽  
Zs. Ács ◽  
G. B. Makara ◽  
K. Mihály
Keyword(s):  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Release Mechanism ◽  
Significant Elevation ◽  
Plasma Corticosterone Level ◽  
Corticosterone Concentration ◽  
Corticotrophin Releasing Factor ◽  
Adrenocortical Response ◽  
The Difference ◽  
Acth Release

Twenty-four hours after the last of 14 daily injections of ACTH, the administration of ether, histamine, 1% formalin, or lysine-8-vasopressin produced no rise in the plasma corticosterone level in rats but raised it significantly in saline-treated control animals. As assayed by the plasma corticosterone concentration, ACTH release was found to be inhibited when hypophyseal–adrenocortical responsiveness was not impaired and the peripheral corticosterone level was normal or less than normal. Endotoxin induced nearly the same statistically significant elevation in the ACTH-treated and saline-treated animals. It would appear that it is the high corticosterone level produced by the last ACTH injection that suppresses the corticotrophin-releasing factor (CRF) 24 h later (feedback action) when this level returns to normal or less than normal; and that certain stressors liberate CRF whereas others do not. An explanation for the latter assumption may be found either in the difference in intensity between the stimuli or, more probably, in that the high corticosterone level inhibits the ACTH release mechanism for certain individual stressors, but not for others.

Reduced adrenocortical function and increased thyroid function in fasted and refed chickens

1983 ◽  
Vol 98 (1) ◽  
pp. 129-135 ◽  
Author(s):  
S. Harvey ◽  
H. Klandorf
Keyword(s):  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Metabolic Effects ◽  
Adrenocortical Function ◽  
Free Access ◽  
Similar Reduction ◽  
Corticosterone Concentration ◽  
Post Feeding ◽  
Access To Food ◽  
Food Consumed

The deprivation of food for 48 h markedly increased (P< 0·001) the corticosterone concentration in the plasma of 7- to 8-week-old chickens. When fasted birds were refed for 2 min or 5 s the corticosterone concentration fell to the level in fed birds within 30 min of refeeding. In fasted and refed birds the plasma corticosterone concentration remained lowered for at least 150 min after a 2-min period of refeeding, whereas in birds refed for 5 s the concentration had increased within 120 min to that in fasted birds. When fasted birds were refed 1, 5, 15 or 30 g diet the corticosterone level was again markedly reduced (P< 0·001) within 45 min of refeeding. The magnitude of this post-feeding decline was unrelated to the amount of food eaten, although its duration was; the level in birds refed 1, 5 or 15 g food increasing to that in fasted birds within 90, 135 and 225 min respectively. The corticosterone level in birds refed 30 g diet remained reduced for at least 225 min but increased to that in fasted birds 24 h after refeeding. The initial decline in the corticosterone concentration was unrelated to the consumption of food, since a similar reduction in the corticosterone level was observed in fasted birds which were given the sight of food but prevented from eating it by Perspex lids attached to the food troughs. This initial decline in the corticosterone level was not a result of stress, as it did not occur in fasted control birds. These results suggest that the adrenocortical changes in fasted and refed birds is initially mediated by a conditioned neural stimulus (reinforcement) and is maintained as a result of peripheral metabolic effects of ingested food. In fasted chickens the concentration of plasma tri-iodothyronine (T3) was greatly reduced (P<0·001) in comparison with fed birds. When fasted birds were refed for 2 min or with 5, 15 or 30 g diet, the level of plasma T3 was increased (P < 0·05) 90 min after refeeding although not to the level in birds which had free access to food. The magnitude and duration of this increase was related to the amount of food consumed and was not observed in birds refed for 5 s or with 1 g food or in fasted birds given sight of but not access to food.

scholarly journals Pregnancy-induced adaptations of the central circadian clock and maternal glucocorticoids

2015 ◽  
Vol 228 (3) ◽  
pp. 135-147 ◽  
Author(s):  
Michaela D Wharfe ◽  
Peter J Mark ◽  
Caitlin S Wyrwoll ◽  
Jeremy T Smith ◽  
Cassandra Yap ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Hpa Axis ◽  
Clock Genes ◽  
Circadian Variation ◽  
Maternal Plasma ◽  
Plasma Corticosterone ◽  
Plasma Acth ◽  
Corticosterone Concentration ◽  
Physiological Adaptations ◽  
Acth Concentration

Maternal physiological adaptations, such as changes to the hypothalamic–pituitary–adrenal (HPA) axis, are central to pregnancy success. Circadian variation of the HPA axis is dependent on clock gene rhythms in the hypothalamus, but it is not known whether pregnancy-induced changes in maternal glucocorticoid levels are mediated via this central clock. We hypothesized that hypothalamic expression of clock genes changes across mouse pregnancy and this is linked to altered HPA activity. The anterior hypothalamus and maternal plasma were collected from C57Bl/6J mice prior to pregnancy and on days 6, 10, 14 and 18 of gestation (term=d19), across a 24-h period (0800, 1200, 1600, 2000, 0000, 0400 h). Hypothalamic expression of clock genes and Crh was determined by qPCR, plasma ACTH concentration measured by Milliplex assay and plasma corticosterone concentration by LC-MS/MS. Expression of all clock genes varied markedly across gestation, most notably at mid-gestation when levels of each gene were elevated. The pregnancy-induced increase in maternal corticosterone levels (by up to 14-fold on day 14) was not accompanied by a parallel shift in plasma ACTH (28% lower on day 14 compared with non-pregnant levels). Moreover, while circadian rhythmicity in corticosterone was maintained up to day 14 of gestation, this was effectively lost by day 18. Overall, our data show that the central circadian clock undergoes marked adaptations throughout mouse pregnancy, changes that are likely to contribute to maternal physiological adaptations. Importantly, however, neither hypothalamic clock genes nor plasma ACTH levels appear to drive the marked increase in maternal corticosterone after mid-gestation.

Effects of trenbolone acetate on adrenal function and hepatic enzyme activities in female rats

1983 ◽  
Vol 98 (1) ◽  
pp. 121-127 ◽  
Author(s):  
K. M. Thomas ◽  
R. G. Rodway
Keyword(s):  
Plasma Corticosterone ◽  
Tyrosine Aminotransferase ◽  
Adrenal Function ◽  
Female Rats ◽  
Hepatic Enzyme ◽  
Corticosterone Concentration ◽  
Trenbolone Acetate ◽  
Phosphoenol Pyruvate ◽  
Corticosterone Treatment ◽  
And Control

The effects of the anabolic steroid trenbolone acetate (TBA) on adrenal function and hepatic enzyme activity have been studied in growing female rats. Treatment with TBA resulted in a decrease in the peak of plasma corticosterone concentration which occurred during the afternoon. The enzymes tyrosine aminotransferase (TAT) and phosphoenol-pyruvate carboxykinase were measured in the livers of treated and control rats. Activities of both enzymes were maximal at 22.00 h, but that of TAT was reduced in TBA-treated rats. After injection of ACTH, TBA-treated rats showed a smaller increase in plasma corticosterone than did controls. Treatment with TBA did not affect the induction of TAT activity after corticosterone treatment. All TBA-treated rats grew significantly faster than controls and the possible relevance of this reduced adrenal function to the increased growth rate is discussed.

Effects of passive immunization with antisomatostatin serum on plasma corticosterone concentrations in young domestic cockerels

1988 ◽  
Vol 116 (2) ◽  
pp. 179-183 ◽  
Author(s):  
A. Cheung ◽  
S. Harvey ◽  
T. R. Hall ◽  
S.-K. Lam ◽  
G. S. G. Spencer
Keyword(s):  
Passive Immunization ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Experimental Manipulation ◽  
Adrenocortical Function ◽  
Central Component ◽  
Corticosterone Concentration ◽  
Peak Response ◽  
Control Value ◽  
Normal Sheep Serum

ABSTRACT Young cockerels (6–8 weeks old) were injected with serum from sheep immunized against somatostatin-14 (anti-SRIF) or normal sheep serum (NSS). Blood samples were withdrawn periodically for the determination of plasma corticosterone concentration by radioimmunoassay. With frequent (every 10 min) sampling, NSS-treated control animals exhibited increased plasma corticosterone levels, presumably as a stress response to the experimental manipulation. Anti-SRIF stimulated a much greater increase in plasma corticosterone concentrations and a peak response was observed within 10 to 20 min, when the plasma corticosterone level reached more than twice that of the corresponding control value. With less frequent sampling, plasma corticosterone increased with anti-SRIF administration to as much as nine times the corresponding control value, and the peak response occurred much later. Under pentobarbitone anaesthesia, which itself increased basal corticosterone concentrations, anti-SRIF treatment promoted further increases in plasma corticosterone levels although to a smaller magnitude compared with conscious birds. The results suggest that endogenous somatostatin may play a role in the regulation of adrenocortical function in the domestic fowl. The mechanism of response may involve a central component. J. Endocr. (1988) 116, 179–183

EFFECT OF STRESS AND ENVIRONMENTAL TEMPERATURE ON ADRENAL FUNCTION IN RANA ESCULENTA

1973 ◽  
Vol 57 (3) ◽  
pp. 385-391 ◽  
Author(s):  
M. JURÁNI ◽  
K. MURGAŠ ◽  
L. MIKULAJ ◽  
F. BABUŠÍKOVÁ
Keyword(s):  
Environmental Temperature ◽  
Corticosterone Level ◽  
Rana Esculenta ◽  
Plasma Corticosterone ◽  
Plasma Corticosterone Level ◽  
Corticosterone Concentration ◽  
Stress Changes ◽  
Prolonged Immobilization ◽  
Rapid Activation ◽  
Environmental Temperatures

SUMMARY The effect of immobilization for 60 min on the adrenal activity of frogs (Rana esculenta) was studied by measuring corticosterone in plasma and corticosterone and catecholamines in adrenorenal homogenates. An increase in plasma corticosterone and in noradrenaline in the adrenorenal homogenate was observed after immobilization for 5 min and there was further increase after prolonged immobilization. However, there was no change throughout the period of immobilization in the corticosterone and adrenaline content of the adrenorenal homogenates. When frogs were exposed to various environmental temperatures the resting plasma corticosterone level did not change at temperatures below 20 °C, but rose significantly at temperatures above 20 °C. No increase in plasma corticosterone concentration occurred at 1 °C after corticotrophin (ACTH) administration. At higher temperatures (up to 30 °C) a significant correlation was found between plasma corticosterone levels after ACTH administration and environmental temperature. No further increase in plasma corticosterone took place at temperatures up to 40 °C. The results indicate a rapid activation of both the interrenal and chromaffin components of the adrenal gland in Rana esculenta when subjected to this type of stress. Changes in plasma corticosterone levels resulting from changes in environmental temperature may be either an expression of specific changes in steroidogenesis of the adrenals, or of the entire metabolic activity of the organism.

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