Adrenal Hyperaemia Caused by Corticotrophin

Maier, Felicitas; Staehelin, Matthys

doi:10.1530/acta.0.0580613

Cited by 8 publications

(6 citation statements)

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“…1) confirms previous reports (Maier & Staehelin, 1968;Müller, 1978;Akana, Shinsako & Dallman, 1980;Vazir et al 1981). Much of the increase was presumably due to the increased blood content of the glands rather than hypertrophy (Pudney, Price, Whitehouse & Vinson, 1984).…”

Section: Effects Of Different Doses Of Acthsupporting

confidence: 89%

Studies on the mechanisms of ACTH-induced inhibition of aldosterone biosynthesis in the rat adrenal cortex

Abayasekara

Vazir²,

Whitehouse³

et al. 1989

Journal of Endocrinology

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In rats, chronic treatment with high doses of ACTH (10-40 micrograms/100 g body weight per day) leads to a marked reduction in aldosterone synthesis by adrenal capsules. The possibility that this inhibition is secondary to a decrease in plasma potassium levels or in renin angiotensin system (RAS) activity has been explored. The effects of chronic ACTH treatment were compared in (I) animals in which the endogenous RAS activity was stimulated by restricting dietary sodium intake, (II) animals in which plasma angiotensin II was increased by infusion from implanted osmotic minipumps and (III) animals which received supplementary potassium and in which hypokalaemia was prevented. In all cases, rates of aldosterone biosynthesis in vitro by adrenal capsules were decreased in ACTH-treated animals to an extent similar to those in untreated controls. In addition, ACTH treatment of hypophysectomized rats resulted in a similar inhibition of aldosterone biosynthesis to that found in sham-operated controls. It may be concluded that the ACTH-induced reduction of aldosterone biosynthesis is independent of the secretion of other pituitary hormones, and cannot be simply ascribed to either a reduction in RAS activity or in plasma potassium levels. The results are consistent with the view that the effects of chronic ACTH treatment are mediated by a direct action on the zona glomerulosa cell, which leads to its transformation into a zona fasciculata-like form.

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Section: Effects Of Different Doses Of Acthsupporting

confidence: 89%

Studies on the mechanisms of ACTH-induced inhibition of aldosterone biosynthesis in the rat adrenal cortex

Abayasekara

Vazir²,

Whitehouse³

et al. 1989

Journal of Endocrinology

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“…In fact, the latter was used by Masui & Garren (1970) who demonstrated that the vehicle (16% gelatin solution) was not better than 0.9% NaCl. On the other hand, Maier & Staehelin (1968) using the long acting ACTH of Organon, Cortrophin-Zn, a zinc derivative of ACTH, indued morphological changes similar to the one described here.…”

Section: Discussionsupporting

confidence: 75%

“…This enlargement, as well as the changes in extracellular amorphous and fibrous material may be due to the high level of glucocorticoid hormone prevalent in and around the sinu¬ soids. Indeed, Maier & Staehelin ( 1968) have shown a parallelism between the adrenal blood content and the plasma corticosterone level, in hypophysectomized rats treated with Zn-ACTH. It is conceiv¬ able that a chronic hypersécrétion of ACTH may lead to pathological haemorrhagic conditions of the adrenals such as those observed in humans in the socalled adrenal insufficiency condition, Schwartzman-Sanarelli syndrome and WaterhouseFriederichsen syndrome (Greendyke 1965;Pataki 1967;Batzenschlager & John 1968).…”

Section: Discussionmentioning

confidence: 95%

“…It is conceiv¬ able that a chronic hypersécrétion of ACTH may lead to pathological haemorrhagic conditions of the adrenals such as those observed in humans in the socalled adrenal insufficiency condition, Schwartzman-Sanarelli syndrome and WaterhouseFriederichsen syndrome (Greendyke 1965;Pataki 1967;Batzenschlager & John 1968). In fact, adre¬ nal hyperaemia (Moon 1937;Maier & Staehelin 1968) or haemorrhage (Selye & Stones 1950;Ingle 1951;Wilbur & Rich 1953;Bavaud 1973) have been produced by ACTH treatment in the rat.…”

Section: Discussionmentioning

confidence: 99%

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Effect of ACTH on the proliferative and secretory activities of the adrenal glomerulosa

Payet

Lehoux

Isler

1980

Acta Endocrinologica

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The mitotic, trophic and secretory responses of the adrenal cortex to various preparations and doses of ACTH were investigated in the rat. 1-24-ACTH depot (Synacthen) elicited the highest mitotic and trophic stimulation. The mitotic stimulation occurred exclusively in the glomerulosa, the trophic stimulation occurred mainly in the fasciculata-reticularis and the functional stimulation was found in both, as indicated by the plasma aldosterone and corticosterone levels. The functional changes occurred first, the trophic changes later. Large doses of ACTH inhibited cell proliferation in the fasciculata. The trophic action consisted in an enlargement of the adrenal, to a great extent in the fasciculata-reticularis, and to a lesser extent in the glomerulosa. This enlargement was due partly to parenchymal cell hypertrophy, but also and mostly to stromal hypertrophy, especially hyperaemia. The largest dose of ACTH caused a considerable widening of the sinusoids of the fasciculata-reticularis and medulla, and possibly caused a loss of parenchymal cells in the reticularis. These effects are reminiscent of the well documented haemorrhagic conditions of the adrenals in humans.In a previous work dealing with the hyperplastic stimulation of the adrenal glomerulosa by various hormones, we had found little effect of ACTH on the glomerulosa (Payet 8c Isler 1976). When we later examined the zona fasciculata, which is the acknowledged target tissue of ACTH, paradoxical¬ ly we found no effect on this layer. Therefore, we decided to investigate this lack of effect in more detail, using various plain and long acting ACTH preparations and doses. Our findings are reported in this paper. They again are paradoxical since we found a considerable hyperplastic stimulation of the zona glomerulosa and a lack of such stimulation of the fasciculata. We also investigated the relation¬ ship between mitotic and secretory activity of the cortical layers. Materials and MethodsThe general procedure was the same as that described in a previous article (Payet & Isler 1976). Two months old female hooded rats were kept in individual cages, fed purina laboratory chow and water ad libitum, and han¬ dled daily during the week prior to the experiment to minimize the stress due to manipulation under treat¬ ment.Plain 1-39-ACTH was obtained from Schwartz-Mann Biochemical division of Picker Nuclear, Montreal, as a porcine preparation of 70 IU/mg potency; a similar preparation from Nordic Pharmaceuticals Ltd. was also used (Duracton); it is available in aqueous solution con¬ taining carboxymethyl-cellulose, dextrose and phenol.1-39-ACTH Depot was the Acthar Gel (H.P.) prepara¬ tion of the Armour Pharmaceutial Company and consists in a highly purified ACTH in an aqueous solution of 16% gelatin, 0.15% phenol and 0.1% cysteine.

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“…of the glands, since it is difficult to assess from morphological observations alone how much growth has taken place. In acute experiments, Maier and Staehelin (1968) showed that while ACTH almost doubled the blood content of the adrenal within 24 hours, there was also an increase in net adrenal weight. Payet et al (1980) found that although the enlargement of the adrenal after 2 days of ACTH treatment was greatest in the fasciculata and reticularis zones, it was mainly caused by stroma!…”

Section: Effects On Adrenal Sizementioning

confidence: 98%

Effects of chronic ACTH stimulation on the morphology of the rat adrenal cortex

Pudney

Price²,

Whitehouse³

et al. 1984

Anat. Rec.

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The effects of chronic ACTH treatment (Depot Synacthen, 100 micrograms/day) on the morphology of the rat adrenal were studied in animals treated for 1 to 18 days. The gross weight of the adrenal increased up to tenfold, but although mitotic figures were seen after 3 days in the glomerulosa region, most of this is attributable to a vast increase in blood content. After 3 days of treatment the sinusoids in the reticularis became extremely dilated, and red blood cells penetrated the endothelial wall to become tightly packed around the cortical cells. This led to the gross distortion of the organization of the cortical tissue and after 7 days the cells in the reticularis region were isolated from each other by the continual infiltration of red blood cells. These changes gradually progressed outward so that other regions of the cortex became similarly affected. Eventually the cord-like arrangement of the fasciculata was disrupted. After 18 days of treatment, most of the cortex was involved and only a very thin layer of cells lying beneath the adrenal capsule was seemingly unaffected. Another major effect of corticotrophin treatment was the gradual loss of cellular differentiation, particularly of glomerulosa cells. Although the glomerulosa appeared normal after 1 day of treatment, cells of the fasciculata abut directly on the connective tissue capsule following 3 days of ACTH administration. Eventually glomerulosa cells disappeared almost completely, although there was no sign of cellular necrosis. It is likely that glomerulosa cells are transformed into fasciculata-type cells under ACTH treatment. This interpretation is consistent with functional changes that occur at the same time, including the loss of aldosterone synthetic capacity.

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Adrenal Hyperaemia Caused by Corticotrophin

Cited by 8 publications

References 0 publications

Studies on the mechanisms of ACTH-induced inhibition of aldosterone biosynthesis in the rat adrenal cortex

Studies on the mechanisms of ACTH-induced inhibition of aldosterone biosynthesis in the rat adrenal cortex

Effect of ACTH on the proliferative and secretory activities of the adrenal glomerulosa

Effects of chronic ACTH stimulation on the morphology of the rat adrenal cortex

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