The effects of corticosterone, 18-OH-DOC, DOC and 11β-hydroxyprogesterone on the adrenal pituitary axis of the stressed rat

Kraulis, I.; Traikov, H.; Li, M.P.; Birmingham, Marion K.

doi:10.1016/0022-4731(73)90019-8

Cited by 26 publications

(11 citation statements)

References 25 publications

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“…The same laboratory had previously shown that rats treated for 3 days with 18-hydroxydeoxycorticosterone (1 mg/100 g body wt. twice a day) responded on the third day with abnormally high plasma corticosterone concentrations and in vitro corticosterone production in response to ether stress (Kraulis et al, 1973). Our experiments confirm that 18-hydroxydeoxycorticosterone is capable of exaggerating stress-induced ACTH release, and this is probably due to an interference with the fast feedback mechanism of corticosterone.…”

Section: Discussionsupporting

confidence: 73%

“…Furthermore, Kraulis et al (1973) found that adrenal glands removed from rats treated with 1 1/3-hydroxyprogesterone, 11-deoxycorticosterone, 1 8-hydroxydeoxycorticosterone or corticosterone (1 mg/100 g body wt. for 3 days) responded to ACTH stimulation in vitro with a similar increase in in vitro corticosterone production to that in control animals.…”

Section: Discussionmentioning

confidence: 99%

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Structure‐activity Relationship of Various Corticosteroids on the Feedback Control of Corticotrophin Secretion

Jones

Tiptaft

1977

British J Pharmacology

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1 Several steroids occurring in the pathway of corticosteroid biosynthesis were investigated for their ability to exert a fast or delayed feedback inhibition of stress-induced release of corticotrophin. Rats were injected subcutaneously with vehicle or a steroid either 10 min (fast feedback) or 4 h (delayed feedback) before they were subjected to stress which consisted of a 2 min exposure to ether vapour. 2 Changes in plasma corticosterone concentration and in vitro corticosterone production by excised adrenal glands were used as indices of corticotrophin release. 3 Among the steroids tested only 1 lB, 21-dihydroxypregn-4-ene-3, 20-dione (corticosterone) and 1I#, 17a, 2 1-trihydroxypregn-4-ene-3, 20-dione (cortisol) inhibited the stress response 10 min after their administration. Therefore, it appears that the fast feedback mechanism is limited to steroids with a 2 1-hydroxyl and a 1 lp-hydroxyl group.4 In contrast, many steroids caused inhibition of the stress response 4 h after their administration. These steroids were corticosterone, cortisol, 21-hydroxypregn-4-ene-3, 20-dione (1 1-deoxycorticosterone), 17a, 21-dihydroxypregn-4-ene-3, 20-dione (1 l-deoxycortisol), 1 1B-hydroxypregn-4-ene-3, 20-dione (11/p-hydroxyprogesterone) and 11p, 17a-dihydroxypregn-4-ene-3, 20-dione (11p, 17a-dihydroxyprogesterone). Thus, either the 21-hydroxyl group (e.g. 1 1-deoxycorticosterone) or the 1 1,-hydroxyl group (e.g. 11/p-hydroxyprogesterone) is sufficient for delayed feedback activity. The 1 lahydroxyl group, e.g. 1 la, 17a, 21-trihydroxypregn-4-ene-3, 20-dione (1 1-epicortisol) renders the steroid inactive on both feedback mechanisms. 5 18, 21-Dihydroxypregn-4-ene-3, 20-dione (18-hydroxydeoxycorticosterone) was found to be the only steroid that is secreted by the adrenal gland of the rat in quantities sufficient to cause exaggeration of the stress-induced release of corticotrophin. This steroid has been implicated as a possible hypertensive agent, and its role in the control of corticotrophin secretion is discussed here.

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Structure‐activity Relationship of Various Corticosteroids on the Feedback Control of Corticotrophin Secretion

Jones

Tiptaft

1977

British J Pharmacology

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“…It has been shown previously [13,17] that neither !7a-OH-progesterone nor 11-epicortisol modifies the adrenocortical response to ACTH by becoming involved in the biosynthetic pathway or by substrate inhibition. More likely, it is thought, would be a conversion or metabolism of the steroids at the level of the hypothalamus or anterior pi tuitary gland.…”

Section: Discussionmentioning

confidence: 99%

The Combination of 17α-Hydroxyprogesterone and 11-Epicortisol Prevents the Delayed Feedback Effect of Natural and Synthetic Glucocorticoids

Nicholson¹,

Mahmoud

Sutanto

et al. 1986

Neuroendocrinology

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Subcutaneous injection of 400 µg/100 g body weight of corticosterone (B) 2 h previously in male rats prevented the stress response, as assessed by the ability of adrenal glands removed from these animals to produce endogenous B. Two injections of a combination of 17α-hydroxyprogesterone and 11-epicortisol, the first given 30 min before and the second with the B, were able to block this inhibitory effect on the stress response. Neither of the steroids alone was effective in this regard. The combination was also effective against the early delayed feedback effects of 400 µg/100 g body weight cortisol, prednisolone or beclomethasone dipropionate in the same system. The minimum effective dose for reversal of feedback by B or beclomethasone dipropionate (2 mg/100 g body weight of each antagonist) was lower than that required for the same effect against prednisolone or cortisol (5 mg/100 g body weight). Previous injection of B also abolished the ability of anterior pituitary gland fragments to respond to corticotropin-releasing factors (CRFs) added in vitro, an effect which was not abolished by the injection of the combination of putative antagonistic steroids. From experiments designed to measure the ability of 17α-hydroxyprogesterone and 11-epicortisol to compete with ³H-corticosterone in binding to macromolecular components in hypothalamic, hippocampal and pituitary cytosolic preparations, it was deduced that the competition seen in the hypothalamic and hippocampal, rather than the pituitary, preparations was in better accord with the effect seen on the stress response. These results, taken together with our studies of the effects of the two steroids on CRF release from the hypothalamus in vitro, suggest that the site of action of 17α-OH-progesterone and 11-epicortisol is at the hypothalamus (and/or higher centres) and not at the pituitary gland.

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“…Corticosterone, but not 18OH-DOC, causes feedback regulation of ACTH. 74 " Since there is no underutilization of DOC precursor, excess DOC secretion does not occur.…”

Section: Imentioning

confidence: 99%

Dahl salt-susceptible and salt-resistant rats. A review.

Rapp¹

1982

Hypertension

342

210

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strain)* to the hypertensive effect of high salt diet. In this review "salt" will always mean NaCl.t Selective BreedingIn the 1950s, Meneely and coworkers studied the effects of high salt diet on the blood pressure of rats. Meneely and Ball 5 reviewed the work, showing that for a large group of rats the average blood pressure of the group was positively and linearly related to the percentage of NaCl in the diet between 0 and 10% NaCl. Moreover, they remarked that "there was quite a marked degree of individual variation" in the response of blood pressure to salt. This work was carried out on Sprague-Dawley rats that were presumably randombred.•A nomenclature committee of the International Society of Hypertension has stated that Dahl salt-sensitive (or salt-susceptible) rats should be designated DS and Dahl salt-resistant rats should be designated DR (see ref. I). This nomenclature is specifically not used in this review, and its use. except as noted below, is discouraged. In DahTs original work in 1962 and for 14 years until his death. Dr. Dahl called the strains S and R. There is no need to replace that historic precedent. The nomenclature committee specifically states that they were naming "hypertensive rat strains with stable hypertension which had been inbred (brother-sister mating) for at least 20 generations" (ref. \>. Apparently they were naming inbred strains under development at Brookhavcn National Laboratory since Dr. Dahl's death in November, 1975. No fully inbred rats were supplied to investigators from the Brookhaven colony because they do not exist (yet). What was supplied were rats from colonies of S and R rats separate from the inbreeding program and maintained as Dahl had done for many years by selective breeding, avoiding inbreeding where possible. Thus, the use of DS and DR implies the use of specific inbred strains which do not exist. If and when such strains from Brookhavcn become available, these specific strains of inbred S and R rats can be referred to as DS and DR. tSodium in the diet is expressed in two ways in the literature, either as % Na+ or % NaCl The latter assumes that all the Na+ is present as NaCl, % NaCl means grams of NaCl per 100 grams of food. In most of the literature reviewed, sodium was expressed as % NaCl, and so this will be used throughout the review. Where the original article gave data in % N a + . this will be given followed by the % NaCl so that diets can always be compared on the same basis (% NaCl = 2.54 times % Na + ).A survey of commercial rat chows shows that they contain close to 1% NaCl, and so "normal salt diet" will refer to l%NaCl in the food. Two diets were introduced by Dahl during his work with S and R rats: 8% NaCl diet referred to as "high salt diet"; and 0.3 to 0.4% NaCl diet referred to as "low salt diet." Note that with this arbitrary nomenclature, low salt diet has only somewhat less than half the salt content of normal diet. Where a diet was fed that contained insufficient salt for optimum growth, this will be called sodium-deficient diet. The m...

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The effects of corticosterone, 18-OH-DOC, DOC and 11β-hydroxyprogesterone on the adrenal pituitary axis of the stressed rat

Cited by 26 publications

References 25 publications

Structure‐activity Relationship of Various Corticosteroids on the Feedback Control of Corticotrophin Secretion

Structure‐activity Relationship of Various Corticosteroids on the Feedback Control of Corticotrophin Secretion

The Combination of 17α-Hydroxyprogesterone and 11-Epicortisol Prevents the Delayed Feedback Effect of Natural and Synthetic Glucocorticoids

Dahl salt-susceptible and salt-resistant rats. A review.

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