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

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.

1983 ◽  
Vol 244 (2) ◽  
pp. E186-E189 ◽  
Author(s):  
M. M. Wilson ◽  
S. E. Greer ◽  
M. A. Greer

To determine the interactions among the determinants of ACTH secretion, we examined the influence of circadian rhythmicity on glucocorticoid suppression of ACTH. Adrenalectomized rats were injected with the same amount of corticosterone at 0900 and 1800 h, and plasma ACTH concentrations were determined under basal conditions and after a standard ether stress. At 0900 h, corticosterone suppressed both basal and stress-induced plasma ACTH concentrations. At 1800 h, the same treatment suppressed basal ACTH secretion but not the stress-induced rise. Although the same amount of corticosterone was injected at both times of day, the plasma corticosterone concentration 5 min after injection was higher at 1800 h than at 0900 h. This study indicates that there is a nycterohemeral difference in feedback suppression of stress-induced ACTH secretion by a given dose of corticosterone. The daily variation in feedback inhibition may be due to the additive effect of the evening surge stimulus and the stress stimulus that together override the feedback signal.


2015 ◽  
Vol 228 (3) ◽  
pp. 135-147 ◽  
Author(s):  
Michaela D Wharfe ◽  
Peter J Mark ◽  
Caitlin S Wyrwoll ◽  
Jeremy T Smith ◽  
Cassandra Yap ◽  
...  

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.


1981 ◽  
Vol 241 (1) ◽  
pp. R21-R24 ◽  
Author(s):  
R. G. Doell ◽  
M. F. Dallman ◽  
R. B. Clayton ◽  
G. D. Gray ◽  
S. Levine

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.


1990 ◽  
Vol 258 (1) ◽  
pp. E65-E70 ◽  
Author(s):  
A. R. Gwosdow ◽  
M. S. Kumar ◽  
H. H. Bode

The effect of varying doses of purified human interleukin 1 (IL-1) on rectal temperature (Tr), hypothalamic corticotropin-releasing hormone (CRH), pituitary and plasma adrenocorticotropic hormone (ACTH), and plamsa corticosterone was examined in intact male rats at 24 degrees C; plasma ACTH and corticosterone responses were also studied in hypophysectomized rats. In addition, IL-1-induced changes in corticosterone concentration were investigated by means of adrenal organ cultures. Tr was measured with thermocouples. CRH and ACTH levels were determined by radioimmunoassay, and corticosterone by protein-binding assay. Intravenous administration of IL-1 (0.063-1.0 ng) resulted in hyperthermia, which began 20 min postinjection and continued for an additional 30 min. IL-1 at a dose of 0.5 ng resulted in no change in hypothalamic CRH, pituitary ACTH, or plasma ACTH levels compared with saline-treated rats. Plasma corticosterone was significantly (P less than 0.05) elevated 30 min after IL-1 administration and returned to control levels after 1 h. The higher dose of IL-1 (1.0 ng) did not affect hypothalamic CRH content, but pituitary ACTH began to rise at 15 min and was significantly (P less than 0.05) elevated 30 min after injection. Rats receiving this dose displayed elevated (P less than 0.05) plasma ACTH and corticosterone levels 30 and 60 min postinjection. No change in plasma corticosterone was observed in hypophysectomized rats administered either 1 ng of IL-1 or 1 microgram of recombinant IL-1 beta (rIL-1 beta); adrenal organ cultures treated with IL-1 (10(-11) M) responded similarly.(ABSTRACT TRUNCATED AT 250 WORDS)


1981 ◽  
Vol 240 (2) ◽  
pp. E131-E135
Author(s):  
M. E. Thompson ◽  
G. A. Hedge

Systemic indomethacin (Ind) administration decreased prostaglandin F (PGF) content of the rat adrenal to less than 1.4 pg/mg. This was less than 5% of the adrenal PGF content in the gelatin-treated (Gel) control group (34 pg/mg). Basal plasma corticosterone levels were increased by the Ind treatment. Since the calculated metabolic clearance rate for corticosterone was unchanged, this increase was attributed to an enhanced adrenal secretion rate that was secondary to elevated plasma ACTH concentration. Ether exposure in the presence of Ind did not stimulate a normal rise in plasma corticosterone or adrenal corticosteroidogenesis. Adrenal responsiveness to exogenous ACTH was reduced after Ind treatment. There was a normal rise in plasma ACTH levels following ether exposure confirming the adrenal as the site of inhibition. Systemic Ind treatment thus appears to have two sites of action in altering plasma corticosterone levels: 1) a direct effect on the adrenal, inhibiting normal secretion in response to acute elevations of plasma ACTH, and 2) an action at the pituitary or hypothalamic level, eliciting an increase in basal ACTH secretion.


1979 ◽  
Vol 83 (1) ◽  
pp. 1-16 ◽  
Author(s):  
A. SZAFARCZYK ◽  
G. IXART ◽  
F. MALAVAL ◽  
J. NOUGUIER-SOULÉ ◽  
I. ASSENMACHER

SUMMARY Adrenocorticotrophin (ACTH) and corticosterone in the plasma of adult female rats were measured sequentially at 4 h intervals for 24 h before and after lesions of the suprachiasmatic nuclei or treatment with p-chlorophenylalanine (to inhibit serotonin synthesis). After lesions or p-chlorophenylalanine treatment, the concentrations of ACTH were diminished relative to those in control animals and rhythmic changes could not be detected. However, injection of animals, pretreated with p-chlorophenylalanine, with 5-hydroxytryptophan (60 mg/kg) 8 h before the time when plasma ACTH is maximal in intact animals, stimulated ACTH secretion up to control values. Mean corticosterone concentrations in plasma remained unchanged (after lesions) or increased (after p-chlorophenylalanine). This increase was associated with an increased minimal concentration of corticosterone. After both treatments there was evidence of continued circadian or ultradian rhythms of corticosterone concentration. Locomotor activity of female rats given identical treatment, but without blood sampling, indicated that nocturnal activity was diminished after lesions whereas diurnal activity was enhanced after p-chlorophenylalanine treatment. Periodicity analysis detected the persistence of free-running circadian, and sometimes ultradian activity, rhythms. Adrenalectomy did not alter further the activity pattern observed in rats with lesions. These results therefore support the proposition that both the suprachiasmatic nuclei and the serotoninergic system play an irreplaceable role in the mechanism of ACTH secretory rhythms. The suprachiasmatic nuclei are also important for synchronization of locomotor activity and corticosterone rhythms, which may both persist after the suppression of ACTH rhythms.


1983 ◽  
Vol 98 (1) ◽  
pp. 121-127 ◽  
Author(s):  
K. M. Thomas ◽  
R. G. Rodway

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.


1994 ◽  
Vol 13 (3) ◽  
pp. 89-93 ◽  
Author(s):  
Y. Yamasumi ◽  
T. Shiraishi ◽  
K. Miyashita ◽  
M. Kuroda ◽  
W. Luo ◽  
...  

In order to study the effects of fluctuating infrasound, rats were exposed to traffic noise. Responses of the pituitary adrenocortical system were evaluated by the plasma ACTH and corticosterone concentration. The plasma ACTH concentration increased significantly in rats exposed to fluctuating infrasound at 100 dB and 110 dB (Leq) as compared with the controls. No significant increase of the plasma ACTH concentration was found in rats exposed to 110 dB steady-state infrasound. According to these results, the effect of fluctuating infrasound is greater than that of steady-state infrasound.


1986 ◽  
Vol 112 (3) ◽  
pp. 396-403 ◽  
Author(s):  
Jean Paul Dupouy ◽  
Alain Chatelain

Abstract. CBG and pituitary-adrenal activities were investigated in intact rat foetuses, in newborns spontaneously delivered by vaginal way and in postmature foetuses from mothers with delayed parturition caused by daily progesterone injection from day 20 of gestation. The postmature foetuses had lower body weights and higher adrenal weights on day 22, 23 and 24 of gestation than newborns of the same conceptional age. The corticosterone binding capacity of the plasma as well as the binding capacity of CBG for corticosterone decreased in intact foetuses for the last 3 days of gestation and stayed very low in pups from day 0 to day 8 postpartum. These parameters decreased more slowly in postmature foetuses; however, the differences between the latter and intact foetuses or newborns were not statistically significant. Similar evolution occurred in intact pregnant and suckling females as well as in females with prolonged gestation. The fall in CBG activity in normal rat pups and the subsequent rise in free steroids could explain a sharp decrease in plasma ACTH levels as well as the drop in adrenal and plasma corticosterone concentration. In foetuses with prolonged gestation, the same phenomenon did not occur. Stress conditions produced by maintaining growing foetuses in utero and the development of severe jaundice maintained high ACTH levels. In contrast, the fall in adrenal and plasma corticosterone concentrations in spite of the high level of circulating ACTH could be mainly due to the progesterone inhibition of the steroidogenic activity of the foetal adrenals.


2001 ◽  
Vol 86 (12) ◽  
pp. 5749-5754 ◽  
Author(s):  
Eiji Itagaki ◽  
Sachihiko Ozawa ◽  
Shinya Yamaguchi ◽  
Kenji Ushikawa ◽  
Teruaki Tashiro ◽  
...  

To clarify the mechanism for the potentiation of CRH-induced ACTH response by the infusion of hypertonic saline, we investigated changes in plasma ACTH concentration after infusion of 5% hypertonic saline in five patients with untreated central diabetes insipidus (DI). Basal levels of plasma ACTH and cortisol in the DI group were not significantly different from those in normal control subjects. The infusion of hypertonic saline produced an increase in plasma arginine vasopressin (AVP) in controls, but did not elevate ACTH. However, in patients with DI, the plasma AVP concentration did not change, but circulating ACTH increased 3.6-fold (7.7 ± 1.5 to 23.0 ± 2.7 pmol/liter; P < 0.01), and plasma cortisol also increased significantly (298 ± 99 to 538 ± 124 nmol/liter; P < 0.05). Moreover, a positive correlation was observed between plasma ACTH and osmolality (r = 0.72; P < 0.005). These results indicate that ACTH secretion in DI patients is regulated by a mechanism distinct from that in healthy subjects. It seems possible that the increase in plasma osmolality promotes ACTH secretion in DI patients through AVP and/or urocortin via the hypophyseal portal system, independent of the AVP secretion from magnocellular neurons.


Sign in / Sign up

Export Citation Format

Share Document