Atrophy of the adrenal cortex in the rat produced by administration of large amounts of cortin

Ingle, Dwight J.; Higgins, George M.; Kendall, Edward C.

doi:10.1002/ar.1090710310

Cited by 121 publications

(27 citation statements)

References 9 publications

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“…The high level of circulating corticosterone, the lack of weight gain, and the substantial decrease in adrenal gland weight in the animals that received hormone implants suggest that the paradigm used for analyzing GHRH-R mRNA regulation by corticosteroids mimics the chronic exposure previously demonstrated to inhibit both linear growth (12)(13)(14)(15) and GH release (34). Although it is possible that the increases in pituitary expression of GHRH-R mRNA are caused by the catabolic effects of corticosterone, glucocorticoids remain capable of enhancing GHRH-R gene expression in a primary pituitary cell culture system.…”

Section: Discussionmentioning

confidence: 99%

“…Trunk blood was collected on ice and allowed to clot, and serum was stored at Ϫ20 C for subsequent hormone measurement by RIA. Adrenal gland atrophy (14) and reduced body weight (14,15) have previously been reported as indicators of high circulating levels of corticosterone. Body weight was therefore monitored for each animal throughout the course of the experiment, and the adrenal glands were removed from the sham-operated animals and dissected, and the paired wet weight was measured.…”

Section: In Vivo Effects Of Corticosteronementioning

confidence: 93%

“…In general, glucocorticoids exert a suppressive effect on the GH axis in mammals (13), causing growth retardation in laboratory rats (14,15) and decreased growth rates in chronically treated children (12). In addition, patients with Cushings syndrome, which clinically presents as hypercortisolemia, have almost lost the ability to secrete GH (12).…”

Section: G H Synthesis and Secretion Is Regulated Predomi-mentioning

confidence: 99%

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Glucocorticoids Regulate Pituitary Growth Hormone-Releasing Hormone Receptor Messenger Ribonucleic Acid Expression*

Miller

Mayo

1997

Endocrinology

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Glucocorticoids regulate GH synthesis and secretion by influencing both hypothalamic and pituitary function. With respect to GH-releasing hormone (GHRH), an important GH secretagogue, glucocorticoids are reported not only to suppress hypothalamic GHRH expression but also to augment pituitary responsiveness to GHRH. To investigate further this latter observation, we have determined the effects of this steroid on expression of the GHRH receptor (GHRH-R) gene in the rat pituitary in vivo and in pituitary cells in vitro. Adult male rats were adrenalectomized or sham operated and treated with sc implants of cholesterol or corticosterone. Adrenalectomized animals showed substantially reduced pituitary GHRH-R mRNA levels, when compared with untreated sham-operated animals. Conversely, administration of corticosterone increased pituitary GHRH-R mRNA levels in intact, as well as adrenalectomized rats. We also analyzed the effects of the synthetic glucocorticoid, dexamethasone, on GHRH-R mRNA expression in cultured rat anterior pituitary cells. GHRH-R mRNA was significantly increased by dexamethasone, with a maximal response observed in the presence of 100 nM hormone. This dose of dexamethasone substantially elevated GHRH-R mRNA after 6 h, 12 h, and 24 h of treatment. Dexamethasone did not increase GHRH-R mRNA in the presence of the transcriptional inhibitor actinomycin D, indicating that the predominant effect of the hormone is to increase transcription of the GHRH-R gene. These data demonstrate that GHRH-R mRNA levels are directly stimulated by glucocorticoids, both in the presence and absence of hypothalamic influences, providing a probable explanation for the ability of this steroid to alter pituitary responsiveness to GHRH. (Endocrinology 138: 2458 -2465, 1997) G H SYNTHESIS and secretion is regulated predominantly by the opposing actions of the stimulatory hypothalamic peptide GH-releasing hormone (GHRH) and the inhibitory peptide SS (1, 2). These hormones exert their actions on the somatotrope cells of the anterior pituitary by interacting with specific membrane receptors. Recently, cDNAs for the GHRH receptor (GHRH-R) were cloned and characterized from several mammalian species (3-7). These receptors are members of a growing subfamily of G proteincoupled receptors whose ligands are structurally related peptide hormones (8 -10). The interaction of GHRH with its receptor activates adenylate cyclase through a G proteincoupled pathway, increasing the levels of the second messenger cAMP (3, 9, 10). The critical role of the GHRH-R in stimulating GH release is apparent in the little mouse, a dwarf phenotype resulting from a point mutation in the amino-terminal domain of the protein (4, 9, 10) that leads to loss of receptor function. More recently, human GH deficiency has been associated with a nonsense mutation in the amino-terminal domain of the GHRH-R (11).Corticosteroids are important physiological regulators of GH synthesis and secretion (12). In general, glucocorticoids exert a suppressive effect on the G...

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Section: Discussionmentioning

confidence: 99%

Section: In Vivo Effects Of Corticosteronementioning

confidence: 93%

Section: G H Synthesis and Secretion Is Regulated Predomi-mentioning

confidence: 99%

See 1 more Smart Citation

Glucocorticoids Regulate Pituitary Growth Hormone-Releasing Hormone Receptor Messenger Ribonucleic Acid Expression*

Miller

Mayo

1997

Endocrinology

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“…The decrease of adrenocortical hormone and the atrophy of adrenal cortex produced in normal animals by exogenous corticoid administration are certainly for the most part due to the inhibition of ACTH secretion (Bethune, 1956;Ingle et al, 1938;Sayers and Sayers, 1947;Sayers and Sayers, 1948), because it can be overcome by a small dose of ACTH (Hohlweg and Lasechet, 1959). Large Endocrinol.…”

Section: Discussionmentioning

confidence: 99%

Acute Effect of Morphine Administration on Secretion of Adrenal Corticosterone in Rats

1970

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SynopsisThe purpose of this study is to determine the acute effect of morphine on ACTH secretion and to determine whether morphine has a direct action on the adrenal cortex by the adult female Wistar rat. ACTH was measured by the determination of corticosterone levels in adrenal glands, adrenal venous blood and circulatory blood. It should be emphasized that in this paper, mechanism of secretion of adrenal corticosterone by the acute effect (the early stage action) following morphine administration was described. Even in morphinization with five daily morphine (2mg/100g, B. W., i. p.) injections, the account of acute effect was determined immediately after the final injection of morphine administration. Morphine alone can not act as an inhibitor of ACTH release nor as an inhibitor of ACTH release due to histamine stress, and morphinization can not act to inhibit ACTH release or to block the effect of a histamine stress on the secretion of ACTH in the early stage action of the final morphine administration, as evidenced by corticosterone levels both in adrenal glands and in circulating blood of the intact rats. Morphine (2mg/100g,B. W., i. p.) alone caused stimulation of ACTH release as well as the final morphine injection of morphinization, and pretreatment of the rats with morphine(2mg/100g, B. W., i. p.) could not act to block the effect of a histamine (0.5 mg/ 100g, B. W., i. p.) stress on the release of ACTH in the early stage action of morphine administration. A detailed account of the effect of morphine or morphinization with four daily morphine injections on corticosterone levels both in adrenal and in adrenal venous blood of the hypophysectomized-ACTH-treated rat has been reported. Morphine (2mg/100g, B. W., i. p.) alone or with pretreatment of pentobarbital (1mg/100g, B. W., i.p.) does not directly interfere with the response of the adrenal cortex to exogenous ACTH in the early stage action of morphine administration. Morphinization with four daily morphine (2mg/100g, B. W., i. p.) injections in the early stage action following the directly act on adrenal corticoidogenesis in vivo. These results suggest in the early stage action of morphine administration that morphine acts to stimulate ACTH release at a higher level than the anterior pituitary and does not directly act on adrenal cortex, and that the acute effect of strong stimuli on the rate of ACTH release is not mediated by a decrease in the concentration of circulating adrenal corticosteroids.

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“…(Received 1 April 1964) Ingle, Higgins & Kendall (1938) and Sayers & Sayers (1947) considered that adrenocorticoid production in the rat was dependent upon the secretion of ACTH, which was controlled by the plasma level of adrenocortical hormones. Yates & Urquhart (1962) supported this concept of a biological feed-back mechanism and proposed that the corticoids exerted their depressant action at the hypothalamic level.…”

mentioning

confidence: 99%

Changes of plasma and adrenal corticosterone levels in the rat after repeated stimuli

Stockham¹

1964

The Journal of Physiology

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Atrophy of the adrenal cortex in the rat produced by administration of large amounts of cortin

Cited by 121 publications

References 9 publications

Glucocorticoids Regulate Pituitary Growth Hormone-Releasing Hormone Receptor Messenger Ribonucleic Acid Expression*

Glucocorticoids Regulate Pituitary Growth Hormone-Releasing Hormone Receptor Messenger Ribonucleic Acid Expression*

Acute Effect of Morphine Administration on Secretion of Adrenal Corticosterone in Rats

Changes of plasma and adrenal corticosterone levels in the rat after repeated stimuli

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