In vivo conversion of corticosterone into aldosterone in rats treated with ACTH or submitted to stress

Vecsei, P.; Kessler, H.

doi:10.1007/bf02114168

Cited by 5 publications

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“…In vitro studies showed that ACTH can actually decrease aldosterone production with certain conditions [17,38]. Thus the decline in aldosterone during ACTH may be the result of intraadrenal inhibition of its production [5].…”

Section: Discussionmentioning

confidence: 96%

Mineralocorticoids, salt balance and blood pressure after prolonged ACTH administration in juvenile hypertension

et al. 1978

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The effect of a 5 day ACTH test (40 U/24 h) on plasma aldosterone (aldo), deoxycorticosterone (DOC), plasma renin activity (PRA) and urinary excretion of aldosterone-pH1-conjugate (pH-1-aldo) and tetrahydro-DOC (TH-DOC) was investigated in 8 normotensive children (group I), 8 patients with hypertension of unknown origin (group II), and 4 hypertensive children with dexamethasone suppressible hyperaldosteronism (DSH) (group III). Changes in blood pressure and sodium balance were studied in all groups. Under baseline conditions there was no hormonal difference between group I and II. In contrast, the children in group III had a suppressed PRA and a 1.5--2 fold elevation of aldo and DOC. Plasma DOC and urinary THDOC increased continuously 10--50 fold in all groups during the ACTH test. Aldo rose transiently 2--4 fold on the first day of ACTH and fell subsequently below baseline levels in group I and II. The children with DSH (group III), however, showed an unusual, sustained aldo stimulation with ACTH. PRA decreased significantly after ACTH in group I and II. Sodium retention aTH administration. The highest blood pressure rise was observed in group III (from 124/72 to 139/90 mm Hg). The blood pressure response to ACTH was partly sodium dependent. Although aldo and DOC and sodium retention may contribute to the ACTH induced blood pressure elevation, other factors must play a role.

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Section: Discussionmentioning

confidence: 96%

Mineralocorticoids, salt balance and blood pressure after prolonged ACTH administration in juvenile hypertension

et al. 1978

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“…In a previous study, Vecsei & Kessler (1970) failed to induce any change in the conversion of corticosterone to aldosterone in vivo by the pro¬ longed treatment of potassium-replete rats with sc formalin. In potassium-deficient rats (present ex¬ periments), the administration of formalin or PEG was as effective as the repletion of body potassium (Baumann & Müller 1972;Komor & Müller 1979) in restoring the activity of late steps in aldosterone biosynthesis.…”

Section: Discussionmentioning

confidence: 96%

Stimulation of the conversion of corticosterone to aldosterone by sodium and water depletion of potassium-deficient rats. Comparison of different experimental procedures

Haldy¹,

Müller²

1981

Acta Endocrinologica

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Sodium depletion, hypovolaemia or both were induced in potassium-depleted rats by various experimental protocols in order to study mechanisms involved in the regulation of late steps in aldosterone biosynthesis. The relative effects of such manoeuvres upon aldosterone biosynthesis and upon the plasma renin activity were compared. The conversion of corticosterone to aldosterone by incubated adrenal glands could be stimulated by a factor of 3 to 4 within 48 h by each of the following procedures: feeding on a sodium\x=eow-\ and potassium-deficient diet or on sucrose, water restriction or treatment with furosemide. A 20-fold stimulation was elicited by experimental oedema due to subcutaneous polyethylene glycol solution or formalin. Intermediate responses were obtained by combining the sodium-and potassium-deficient diet with either water restriction or furosemide treatment as well as by the infusion of angiotensin II. Significant increases in the plasma renin activity, which were however not proportional to the stimulation of aldosterone biosynthesis, were seen in rats kept on the sodium-and potassium-deficient diet or treated by furosemide, polyethylene glycol or formalin, but not in rats kept on sucrose or deprived of water. An elevation in the plasma potassium concentration was observed only in the animals treated with water restriction. These results indicate that during potassium deficiency the stimulation of late steps in aldosterone biosynthesis by sodium and water depletion is mediated by the renin-angiotensin system and by an unknown mechanism which enhances the sensitivity of the zona glomerulosa to angiotensin II. Experimental oedema in potassium-deficient rats seems to be a useful model for further investigations of this mechanism.

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Endocrine Functions during Adaptation to Stress

Mikulaj

Mitro

1973

Advances in Experimental Medicine and Biology

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In vivo conversion of corticosterone into aldosterone in rats treated with ACTH or submitted to stress

Cited by 5 publications

References 0 publications

Mineralocorticoids, salt balance and blood pressure after prolonged ACTH administration in juvenile hypertension

Mineralocorticoids, salt balance and blood pressure after prolonged ACTH administration in juvenile hypertension

Stimulation of the conversion of corticosterone to aldosterone by sodium and water depletion of potassium-deficient rats. Comparison of different experimental procedures

Endocrine Functions during Adaptation to Stress

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