1985American Journal of Physiology-Endocrinology and MetabolismRequires access

Effects of mineralocorticoids and glucocorticoids on compensatory adrenal growth in rats

Russell G. Phillips, Carmel Crock, John W. Funder

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Abstract

The rapid compensatory growth seen in the remaining adrenal gland of the rat after unilateral adrenalectomy appears to require a functioning neural arc between the adrenal glands and the hypothalamus, but the role of adrenal or pituitary hormones is unclear. We have examined the effect of several steroids on the compensatory adrenal growth (CAG). Female and male rats (average wt 140 g) were unilaterally adrenalectomized and treated with aldosterone (2.1 micrograms/day), corticosterone (B, 28 micrograms/day), dexamethasone (28 micrograms/day), 9 alpha-fluorocortisol (9 alpha FC, 28 micrograms/day), or deoxycorticosterone (DOC, 28 micrograms/day) by continuous infusion for 3 days and then killed. The growth in the remaining adrenal was compared both with sham-operated rats treated with steroid infusions and with noninfused controls. In rats of this size females have larger adrenals than males; untreated male rats have significantly heavier left than right adrenals. In male rats the extent of CAG after no treatment or treatment with aldosterone B, 9 alpha FC, or DOC depended on the size of the adrenal gland removed. In both male and female rats CAG was not significantly affected by aldosterone, in contrast with a recent report, nor by B, 9 alpha FC, or DOC; no significant CAG was seen after dexamethasone. Taken together, these results and previous reports suggest that neurally mediated activation of pituitary and/or local adrenal growth factors may be responsible for CAG.

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What this paper is about

The rapid compensatory growth seen in the remaining adrenal gland of the rat after unilateral adrenalectomy appears to require a functioning neural arc between the adrenal glands and the hypothalamus, but the role of adrenal or pituitary hormones is unclear. We have examined the effect of several steroids on the compensatory adrenal growth (CAG). Female and male rats (average wt 140 g) were unilaterally adrenalectomized and treated with aldosterone (2.1 micrograms/day), corticosterone (B, 28 micrograms/day), dexamethasone (28 micrograms/day), 9 alpha-fluorocortisol (9 alpha FC, 28 micrograms/day), or deoxycorticosterone (DOC, 28 micrograms/day) by continuous infusion for 3 days and then killed. The growth in the remaining adrenal was compared both with sham-operated rats treated with steroid infusions and with noninfused controls. In rats of this size females have larger adrenals than males; untreated male rats have significantly heavier left than right adrenals. In male rats the extent of CAG after no treatment or treatment with aldosterone B, 9 alpha FC, or DOC depended on the size of the adrenal gland removed. In both male and female rats CAG was not significantly affected by aldosterone, in contrast with a recent report, nor by B, 9 alpha FC, or DOC; no significant CAG was seen after dexamethasone. Taken together, these results and previous reports suggest that neurally mediated activation of pituitary and/or local adrenal growth factors may be responsible for CAG.

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Available abstract

The rapid compensatory growth seen in the remaining adrenal gland of the rat after unilateral adrenalectomy appears to require a functioning neural arc between the adrenal glands and the hypothalamus, but the role of adrenal or pituitary hormones is unclear. We have examined the effect of several steroids on the compensatory adrenal growth (CAG). Female and male rats (average wt 140 g) were unilaterally adrenalectomized and treated with aldosterone (2.1 micrograms/day), corticosterone (B, 28 micrograms/day), dexamethasone (28 micrograms/day), 9 alpha-fluorocortisol (9 alpha FC, 28 micrograms/day), or deoxycorticosterone (DOC, 28 micrograms/day) by continuous infusion for 3 days and then killed. The growth in the remaining adrenal was compared both with sham-operated rats treated with steroid infusions and with noninfused controls. In rats of this size females have larger adrenals than males; untreated male rats have significantly heavier left than right adrenals. In male rats the extent of CAG after no treatment or treatment with aldosterone B, 9 alpha FC, or DOC depended on the size of the adrenal gland removed. In both male and female rats CAG was not significantly affected by aldosterone, in contrast with a recent report, nor by B, 9 alpha FC, or DOC; no significant CAG was seen after dexamethasone. Taken together, these results and previous reports suggest that neurally mediated activation of pituitary and/or local adrenal growth factors may be responsible for CAG.

Key concepts: Internal medicine, Endocrinology, Aldosterone, Corticosterone, Dexamethasone, Adrenalectomy, Adrenal gland, Hormone

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