Hypothalamo‐pituitary Adrenocortical Function in the Rat After Treatment With Betamethasone

Buckingham, Julia C.; Hodges, John R.

doi:10.1111/j.1476-5381.1976.tb07447.x

Cited by 16 publications

(8 citation statements)

References 19 publications

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“…In agreement with these findings, glucocorticoids, in bodi man and experimental animals, have been reported to suppress not only the basal secre tion of ACTH (Copinschi et al, 1975;Buckingham and Hodges, 1976) but also the release of other adenohypophyseal hormones, such as PRL (Copinschi et al, \915\Jobin et al, 1976;Euker et al, 1975;Harms et al, 1975;Schwinn et al, 1976), GH ( Wakabayashi etal, 1971;Copinschi et al, 1975) and TSH {Nicoloff et al, \91Q\Otsuki et al, \913\Ranta, \915\Jobin et al, 1976',Schwinn et al, 1976.…”

Section: Discussionsupporting

confidence: 75%

“…In rats, the profile of the modifications elicited by acute stress now appears to be rather well delineated and characterized by an increased secretion of ACTH (. Buckingham and Hodges, 1976;Engeland et al, 1977), prolactin (PRL), LH and, to a lesser degree, of FSH (Krulich étal., \914\Euker et al, 1975;Turpcn et al, 1976;Du Ruisseau et al, 1978), whereas GH and TSH release is decreased (Collu et al, 1973Krulich et al, 1974;Jobin et a l, 1976;Mueller et al, 1976;Hashimoto et al, 1977;Du Ruisseau et al, 1978).…”

Section: Introductionmentioning

confidence: 99%

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Adenohypophyseal Hormone Response to Chronic Stress in Dexamethasone-Treated Rats

Taché¹,

Ruisseau²,

Ducharme³

et al. 1979

Horm Res

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The influence of dexamethasone treatment on the basal values of corticosterone, GH, prolactin (PRL), LH and FSH, as well as on the adenohypophyseal hormone response to chronic stress was studied in female rats. Dexamethasone acetate (25 µg/100 b.w.), given by gavage twice daily for 10 days, decreased the resting plasma levels of corticosterone, GH, LH and PRL, whereas the FSH titers remained normal. The secretion of ACTH (evaluated indirectly through corticosterone concentrations) and of GH appeared to be most sensitive to the suppressive effect of dexamethasone. The same hormonal response pattern was induced by 8 h of daily immobilization for 10 days, except that ACTH release was enhanced and the plasma LH titers dropped more drastically. Dexamethasone administration in combination with restraint did not alter the characteristic hormonal profile of chronic stress, despite the fact that ACTH secretion was completely blocked. These data suggest that the inhibition of PRL, LH and GH secretion following severe, chronic stress is not causally related to the sustained elevation of plasma ACTH.

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Section: Discussionsupporting

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Adenohypophyseal Hormone Response to Chronic Stress in Dexamethasone-Treated Rats

Taché¹,

Ruisseau²,

Ducharme³

et al. 1979

Horm Res

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“…Similarly, ACTH treatment suppresses aldosterone secretion, and quickly initiates the transformation of glomerulosa into fasciculata cells (Aguilera et al 1981, Pudney et al 1984, Abayasekara et al 1989: prolonged treatment may result in the elimination of the glomerulosa altogether (Vinson 2003). Betamethasone, by contrast, suppresses circulating ACTH, and hence fasciculata function and glucocorticoid secretion (Buckingham & Hodges 1976, Cam & Bassett 1983, Raza et al 2005.…”

Section: Discussionmentioning

confidence: 99%

Eph receptors and zonation in the rat adrenal cortex

Brennan¹,

Chittka²,

Barker³

et al. 2008

Journal of Endocrinology

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Although the zonation of the adrenal cortex has a clear functional role, the mechanisms that maintain it remain largely conjectural. The concept that an outer proliferative layer gives rise to cells that migrate inwards, adopting sequentially the zona glomerulosa, fasciculata and reticularis phenotypes, has yet to be explained mechanistically. In other tissues, Eph receptor (EphR)/ephrin signalling provides a mechanism for cellular orientation and migration patterns. Real-time PCR and other methods were used to determine the possible role of Eph/ephrin systems in the rat adrenal. mRNA coding for several members of the EphR family was detected, but out of these, EphA2 provided the closest parallel to zonal organisation. In situ hybridisation showed that EphA2 mRNA and EphA protein were predominantly located in the zona glomerulosa. Its transcription closely reflected expected changes in the glomerulosa phenotype, thus it was increased after a low-sodium diet, but decreased by pretreatment with the angiotensin-converting enzyme inhibitor, captopril. It was also decreased by ACTH treatment, but unaffected by betamethasone. mRNA coding for ephrin A1, the major ligand for the EphA receptors, was also detected in the rat adrenal, though changes evoked by the various pretreatments did not clearly reflect the expected changes in zonal function. Because the maintenance of cellular zonation requires clear positional signals within the adrenal cortex, these data support a role for Eph forward and reverse signalling in the maintenance of adrenocortical zonation.

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“…Ad ministration of betamethasone has been shown to impair HPA activity in SpragueDawley rats in doses of 0.5-20.0 pg/ml drinking water [23][24][25].…”

Section: Discussionmentioning

confidence: 99%

Long-Term Effects of Betamethasone on Blood Pressure and Hypothalamo-Pituitary-Adrenocortical Function in Spontaneously Hypertensive and Normotensive Rats

Häusler¹,

Girard

Baumann

et al. 1983

Horm Res

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An enhanced hypothalamo-pituitary-adrenocortical (HPA) activity has been described during onset of elevated blood pressure in spontaneously hypertensive rats (SHR). An instability of the HPA axis could thus contribute to the development of hypertension in these animals. Glucocorticoid effects on blood pressure and HPA function were studied therefore in SHR and normotensive Wistar-Kyoto (WKY) and Wistar rats. Beginning at 4 weeks of age, the rats were treated with 0.1 and 0.5 µg betamethasone per milliliter drinking water for 7 weeks. SHR and WKY responded with a significant elevation in average blood pressure. In SHR, mean blood pressure rose from 181.4 ± 3.9 (mean ± SEM) to 203.1 ± 2.8 mm Hg in response to the lower dose of betamethasone and to 209.2 ± 4.0 mm Hg in response to 0.5 µg betamethasone per milliliter drinking water. In WKY, blood pressure increased from 134.4 ± 3.3 to 148.2 ± 3.0 and 157.9 ± 4.5 mm Hg in response to the lower and higher dose of betamethasone, respectively. No significant effect was seen in Wistar rats, where the mean blood pressure values changed insignificantly from 133.8 ± 2.1 to 136.3 ± 3.2 and 135.6 ± 2.4 mm Hg. Stress-induced secretion of corticosterone was significantly suppressed in a dose-dependent manner in all three strains. Stress-induced secretion of adrenocorticotropin was markedly reduced by 0.5 µg betamethasone per milliliter in SHR and by both doses in WKY. No significant effect, however, was seen in Wistar rats. A predisposition to the hypertensiogenic actions of glucocorticoids was found therefore in SHR and WKY, but not in Wistar rats.

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Hypothalamo‐pituitary Adrenocortical Function in the Rat After Treatment With Betamethasone

Cited by 16 publications

References 19 publications

Adenohypophyseal Hormone Response to Chronic Stress in Dexamethasone-Treated Rats

Adenohypophyseal Hormone Response to Chronic Stress in Dexamethasone-Treated Rats

Eph receptors and zonation in the rat adrenal cortex

Long-Term Effects of Betamethasone on Blood Pressure and Hypothalamo-Pituitary-Adrenocortical Function in Spontaneously Hypertensive and Normotensive Rats

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