On the Mechanism of the Adrenal Gland Response to Adrenocorticotrophic Hormone in Hypophysectomized Rats

Staehelin, Matthys; Barthe, P.; Desaulles, P. A.

doi:10.1530/acta.0.0500055

Cited by 22 publications

(12 citation statements)

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“…This was described by Stähelin et al (1965) and confirmed by Overbeek (1981a,b). It was to be expected that the atrophied adrenals would contain only small amounts of AA but the fact that the concentration is well below normal was unexpected and requires an explana¬ tion.…”

supporting

confidence: 64%

Hormonal regulation of ascorbic acid in the adrenal of the rat

Overbeek¹

1985

Acta Endocrinologica

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Fifteen days after hypophysectomy of rats the concentrations of ascorbic acid (AA) in adrenals, liver, blood and urine are lower than in normal rats or in rats 1 day after hypophysectomy. Despite the low levels the percentage AA depletion after administration of ACTH and the subsequent repletion to the pre-ACTH level are normal. Lack of corticosteroids is not the cause of the low AA levels, as shown by experiments in 15 days adrenalectomized rats and in rats treated with low doses of dexamethasone.Fifteen days treatment with high doses of dexamethasone lowered the AA concentrations in adrenals, liver and blood. Treatment with long-acting ACTH maintained adrenal weight but not adrenal and blood AA. A high dose of ACTH lowered these levels. The administration of AA markedly increased the AA levels in blood, but did not normalize its concentration in the adrenals, not even when the size of the adrenals was maintained by treatment with long-acting ACTH. Growth hormone, in particular when administered together with long-acting ACTH, markedly raised the AA concentration in the adrenals but hardly affected the AA blood level. Rats with high blood levels of prolactin induced by pituitary grafts in the kidney also had clearly higher AA levels in adrenals, but not in blood. These results indicate that, although acute AA release from the adrenal is caused by ACTH, AA uptake to a certain concentration is not controlled by the pituitary gland, and above this concentration is promoted by growth hormone and prolactin. In the liver AA release may also be caused by ACTH but the AA production is promoted by other as yet unidentified pituitary factors.In rats 15 days after hypophysectomy the adrenals are markedly atrophied and contain little ascorbic acid (AA) both absolutely (mg/adrenal) and rela¬ tively (mg/100 g adrenal). This was described by Stähelin et al. (1965) and confirmed by Overbeek (1981a,b). It was to be expected that the atrophied adrenals would contain only small amounts of AA but the fact that the concentration is well below normal was unexpected and requires an explana¬ tion.Several explanations are conceivable such as: a decreased supply of AA to the adrenals as a con¬ sequence of an increased urinary excretion of AA; or a decreased production of AA; or a decreased ability of the adrenal to store A A.Such possibilities have been explored in the present study.It was also studied if the lowered corticosterone production in the adrenals influences AA levels in adrenals, blood and liver and if one of the lacking pituitary hormones could be held responsible for the abnormal AA levels in the long-term hypophysectomized rats. Materials and MethodsThe experiments were carried out with male Wistar rats purchased from TNO, Zeist, The Netherlands (body weight about 300 g). Hypophysectomy was performed by the parapharyngeal route. Ascorbic acid (AA) was deter¬ mined in adrenals with the dichlorophenol-indophenol method (USP XX) and in blood, liver and urine with the dinitrophenylhydrazine (DNPH) method described by György &...

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supporting

confidence: 64%

Hormonal regulation of ascorbic acid in the adrenal of the rat

Overbeek¹

1985

Acta Endocrinologica

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“…In skeletal muscle or exocrine glands, where activity is intermittent, the vasodilatation occurring during activity is pronounced and short lasting. In endocrine glands, on the other hand, where activity is continuous over long periods, the accompanying vasodilatation is moderate and prolonged (Holzbauer & Vogt, 1957;Staehelin, Barthe & Desaulles, 1965). In an earlier paper we showed that activation of rabbit adipose tissue by close arterial injection of lipolytic hormones resembles that in endocrine glands in being prolonged and accompanied by a prolonged increase in blood flow (Lewis & Matthews, 1968).…”

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confidence: 98%

The relationship between functional vasodilatation in adipose tissue and prostaglandin

Bowery¹,

Lewis²,

Matthews³

1970

British J Pharmacology

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Summary1. Earlier it had been found that during fat mobilization there was an increased blood flow in the adipose tissue and the tissue contained a vasodilator substance. 2. Extract of an activated fat pad contained 3 to 25 times as much activity as the contralateral resting fat pad. 3. The following findings suggest that the vasodilator substance is prostaglandin E2: (a) It caused contractions of the guinea-pig ileum which were not reduced by mepyramine, but were reduced by atropine.(b) It caused a prolonged vasodilator response when injected closearterially to the epigastric fat pad. (c) It was eluted from a silicic acid column by a solvent system which is known to elute prostaglandins of the E series but not those of the F series.(d) Its indices of discrimination were similar to those of prostaglandin E's when assayed on three different pharmacological preparations.(e) On thin-layer chromatography it behaved more like prostaglandin E2 than E1.4. Neither prostaglandin E1 nor prostaglandin E2 inhibited the release of free fatty acids from the rabbit epigastric fat pad by ACTH1-24. 5. It seems likely that prostaglandin E2 is responsible for the vasodilatation accompanying fat mobilization from adipose tissue.

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“…Hence, dexamethasone blockade has the disadvantage that the action of ACTH on the adrenals and thymus cannot be studied in isolation but only in combination with that of dexamethasone. The method using hypophysectomised rats has the advantage that the base-line levels are so low that they cannot be determined in the system used [18,19]. The dis advantages consist in the loss of all pituitary hormonal functions, together with their peripheral effects, e.g., activication of 1-5-reductase in the adrenal cortex [10].…”

Section: Discussionmentioning

confidence: 99%

Comparison of the Adrenocorticotrophic Effect of a Synthetic Depot Corticotrophin in Normal, Dexamethasone-Blocked, and Hypophysectomised Rats

Barthe¹,

Desaulles²

1971

Horm Res Paediatr

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The ACTH stimulation test for depot preparations was carried out with a synthetic depot corticotrophin (Synacthen Depot®) in normal, dexamethasone-blocked, and hypophysectomised rats. It was found that the response curves (plasma and adrenal corticosterone) were very similar in all three groups, the peak values being somewhat higher in the normal and block dexamethasone-blocked animals. Towards the end of the stimulation test, the normal animals showed a marked deviation from the nycterohemeral rhythm. This change, which complicates the determination of the duration of action of the preparation used, is indicative of a disturbance in the hypothalamo-pituitaryadrenal feedback system. In dexamethasone-blocked animals, the effects of ACTH on the adrenals and thymus cannot be studied in isolation but only in combination with those of dexamethasone. Hence, despite all the technical difficulties involved, the test with hypophysectomised rats is still the method that yields the most easily assessable responses.

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On the Mechanism of the Adrenal Gland Response to Adrenocorticotrophic Hormone in Hypophysectomized Rats

Cited by 22 publications

References 0 publications

Hormonal regulation of ascorbic acid in the adrenal of the rat

Hormonal regulation of ascorbic acid in the adrenal of the rat

The relationship between functional vasodilatation in adipose tissue and prostaglandin

Comparison of the Adrenocorticotrophic Effect of a Synthetic Depot Corticotrophin in Normal, Dexamethasone-Blocked, and Hypophysectomised Rats

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