The Effect of Adrenocorticotrophin on the Nucleic Acid Metabolism of the Rat Adrenal Gland

Imrie, Robert C.; Ramaiah, T. R.; Antoni, F; Hutchison, W. C.

doi:10.1677/joe.0.0320303

Cited by 46 publications

(10 citation statements)

References 21 publications

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“…The obtained results confirm a well-known proliferogenic effect of ACTH on the adrenocortical growth in vivo [14,19,25]. The significant elevation of the MMAR concerned both normal and dwarf mice.…”

Section: Discussionsupporting

confidence: 84%

“…II/08 5 Present address: Dept. of Physiology, Southern Illinois University, Carbondale, IL, USA Offprint requests to: A. Lewifiski, MD (address see above) fibroblast growth factor (FGF), or angiotensin II has been well documented (for review see [10]), however, ACTH can exert both mitogenic effect when applied in vivo [14,19] and antimitotic action in cell [13,20] and organ culture (Sewerynek et al, unpublished observations) of the adrenals. In some other studies the role of prolactin (Prl) [3] and growth hormone (GH) [4,6], as the stimulators of adrenal growth, has been reported.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Stimulatory effect of prolactin on the mitotic activity of the adrenal cortex in snell mice with hereditary dwarfism

Lewiński¹,

Sewerynek²,

Webb

et al. 1988

Res. Exp. Med.

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Effects of thyrotropin (TSH), growth hormone (GH), prolactin (Prl), and ACTH on the proliferation of adrenocortical cells in male Snell dwarf mice and in phenotypically normal male mice from the same strain were examined by means of the colchicine metaphase-arrest technique. After 6 days of treatment, ACTH increased significantly the mean mitotic activity rate (MMAR) of adrenocortical cells in both the normal (nondwarf) and dwarf mice as compared to the corresponding control groups receiving physiologic saline. None of the remaining examined pituitary hormones did exert a mitogenic action on the adrenal cortex of normal mice. It was, however, recorded the significant elevation of the MMAR of the adrenocortical cells in Prl-treated Snell dwarf mice, while TSH and GH did not stimulate mitogenesis. The acquired data corroborates a well-known proliferogenic effect of ACTH on the adrenal cortex in vivo. The increase of the MMAR of the adrenal cortex of Snell dwarfs following Prl-treatment is in agreement with earlier reports.

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Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Stimulatory effect of prolactin on the mitotic activity of the adrenal cortex in snell mice with hereditary dwarfism

Lewiński¹,

Sewerynek²,

Webb

et al. 1988

Res. Exp. Med.

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“…However, hypophysectomy, like dexamethasone treatment, reduces the absolute magnitude of the compensatory growth response (9,14,19,27,32,35), suggesting that either ACTH or NH 2 -terminal POMC-derived peptides could contribute to compensatory growth. Although ACTH treatment increases adrenal weight, the cellular mechanism differs from that of compensatory growth; ACTH stimulates increases in adrenal RNA followed by increases in DNA (16,24), whereas compensatory growth induces rapid increases in DNA ( Fig. 5; Refs.…”

Section: Discussionmentioning

confidence: 99%

Zone-specific cell proliferation during compensatory adrenal growth in rats

Engeland¹,

Ennen²,

Elayaperumal³

et al. 2005

American Journal of Physiology-Endocrinology and Metabolism

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Compensatory adrenal growth after unilateral adrenalectomy (ULA) leads to adrenocortical hyperplasia. Because zonal growth contributions are not clear, we characterized the phenotype of cortical cells that proliferate using immunofluorescence histochemistry and zone-specific cell counting. Rats underwent ULA, sham adrenalectomy (sham), or no surgery and were killed at 2 or 5 days. Adrenals were weighed and sections immunostained for Ki67 (proliferation), cytochrome P-450 aldosterone synthase (P450aldo, glomerulosa), and cytochrome P-450 11␤-hydroxylase (P45011␤, fasciculata). Unbiased stereology was used to count proliferating glomerulosa and fasciculata cells. Adrenal weight increased after ULA compared with sham and no surgery at both time points, and there was no difference between sham and no surgery. However, either ULA or sham increased Ki67-positive cells in the outer fasciculata at both time points compared with no surgery. Outer fasciculata-restricted proliferation is thus associated with adrenal weight gain in ULA but not sham. Experiment repetition using proliferating cell nuclear antigen and bromodeoxyuridine showed similar results. After ULA, adrenal DNA, RNA, and protein increased at both time points, whereas after sham, only adrenal DNA increased at 2 days. Compensatory growth thus results from hyperplasia and hypertrophy, whereas sham induces only a transient adrenal hyperplasia. Dexamethasone pretreatment prevented the increase in adrenal weight after ULA and blocked Ki67 labeling in the outer fasciculata but not zona glomerulosa in all groups. These results clearly show that the outer fasciculata is the primary adrenal zone responsible for compensatory growth, responding to steroid-suppressible stress signals that alone are ineffective in increasing adrenal mass. adrenal cortex; stress; zona fasciculata; zona glomerulosa; adrenal weight COMPENSATORY ADRENAL GROWTH after unilateral adrenalectomy is a well established model of adrenal growth in rodents. The increase in adrenal weight results from cell proliferation, as reflected by increases in adrenal DNA content (11,36). Although increases in weight are restricted to the adrenal cortex and not the medulla (10, 43), it is unclear which cortical zones are responsible for the growth response. Using [ 3 H]thymidine incorporation as an index of proliferation, Reiter and Pizzarello (38) reported increased in vivo labeling in the capsule, glomerulosa, and outer fasciculata after unilateral adrenalectomy in rats, with the largest response in the fasciculata. The finding of proliferation in the capsule and zona glomerulosa in rats after unilateral adrenalectomy is consistent with studies showing increased incorporation of [ 3 H]thymidine in vitro in adrenal capsule-glomerulosa tissue (2). After unilateral adrenalectomy in mice, labeling for proliferating cell nuclear antigen (PCNA) was increased in cells adjacent to the capsule, suggesting that glomerulosa cells were responsible for the growth response in this species (4). However, other studies have su...

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“…It is well documented that in vivo ACTH administration or its hypersecretion causes primarily adrenocortical cellular hypertrophy, which is subsequently followed by hyperplasia (16,31,(49)(50)(51)(52)(53)(54)(55)(56)(57). On the contrary, the direct in vitro effect of ACTH involves inhibition of adrenocortical cell proliferation and stimulation of the cell specialized functions, that is corticosterone secretion (28,34,(58)(59)(60).…”

Section: Discussionmentioning

confidence: 99%

Neuromedin U enhances proliferation of ACTH-stimulated adrenocortical cells in the rat

Trejter

Guidolin²,

Nowak³

et al. 1998

Int J Mol Med

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Abstract. Neuromedin U (NMU) is a brain-gut peptide involved in the regulation of the hypothalamic-pituitaryadrenal axis and adrenocortical cell proliferation. In this study, we investigated the effects of NMU8 (three subcutaneous injections of 6.0 nmol/100 g, 24, 16 and 8 h before autopsy) on the adrenal glands of rats treated for 2 or 4 days with a low (2 μg/100 g body weight/24 h) or a high (8 μg) dose of adrenocorticotropic hormone (ACTH). As revealed by RT-PCR, ACTH treatment did not prevent expression of NMUR1 in rat adrenal cortex. At day 4 of ACTH administration, the weight of adrenals was lower than at day 2. NMU8 administration prevented ACTH-induced increases of adrenal weight at day 2 of the experiment. ACTH plasma concentrations were increased in all ACTH-administered rats. NMU8 administration increased ACTH plasma concentration at day 2 of the lower ACTH dose-treated group while it reduced the ACTH plasma level at day 4 in the higher ACTH dose-administered rats. In all groups of ACTH-treated rats, NMU8 changed neither aldosterone nor corticosterone plasma concentrations. In the zona glomerulosa (ZG), NMU8 increased metaphase index at days 2 and 4 in the lower ACTH dose-treated group and had no statistically significant effect in rats treated with the higher ACTH dose. In the zona fasciculata (ZF), NMU8 administration increased metaphase index at day 2 in the lower ACTH dose-treated group but reduced metaphase index at day 4 in the higher dose ACTHadministered rats. NMU8 reduced the number of cells per unit area both in ZG and ZF at day 2 in the higher ACTH dose-treated rats. In the remaining groups NMU8 did not produce statistically significant changes in the number of cells per unit area. Thus, our findings demonstrate that exogenous NMU may stimulate proliferation primarily of the cortical ZG cells in rats administered with ACTH, although at high doses of exogenous corticotropin an opposite effect occurred.

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The Effect of Adrenocorticotrophin on the Nucleic Acid Metabolism of the Rat Adrenal Gland

Cited by 46 publications

References 21 publications

Stimulatory effect of prolactin on the mitotic activity of the adrenal cortex in snell mice with hereditary dwarfism

Stimulatory effect of prolactin on the mitotic activity of the adrenal cortex in snell mice with hereditary dwarfism

Zone-specific cell proliferation during compensatory adrenal growth in rats

Neuromedin U enhances proliferation of ACTH-stimulated adrenocortical cells in the rat

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