A Sodium-Retaining Influence of Enucleate Rat Adrenal Glands<sup>1</sup>

Gaunt, Richard A.; Renzi, A. A.; Gisoldi, Elvira; Howie, N.

doi:10.1210/endo-81-6-1331

Cited by 18 publications

(4 citation statements)

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“…Tobian & Redleaf (1957) have examined the electrolytes in the aorta of rats administered desoxycorticosterone and salt and found a rise in the sodium content of the vessel wall even in those rats which did not become hypertensive. The conclusion suggested by these facts is that the short-lived sodium retention described in demedullated rats by Gaunt et al (1967) is responsible for the temporary reduction in heart noradrenaline observed in this work.…”

Section: Discussionsupporting

confidence: 51%

“…3. The time course of the pronounced fall in cardiac NA after adrenal demedullation resembles the time course of sodium retention shown by Gaunt, Renzi, Gisoldi & Howie (1967) to follow this operation. It is therefore suggested that it is the change in electrolyte metabolism which is responsible for the abnormality of NA storage; both phenomena occur in demedullated but not in adrenalectomized animals.…”

supporting

confidence: 63%

“…This rules out the possibility that the fall in cardiac NA is directly related to any hypertension which may follow adrenal regeneration, but other findings suggest that it may be caused by changes in electrolyte metabolism which precede and later accompany hypertension. Quite severe sodium retention (in contrast to the sodium loss after adrenalectomy) has been shown (Gaunt et al, 1967) to occur in demedullated male rats given a light sodium load. This retention is most pronounced during the first postoperative week and then subsides gradually.…”

Section: Discussionmentioning

confidence: 97%

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Noradrenaline content of the heart of the adrenal‐demedullated rat

Borchard

Vogt

1970

British J Pharmacology

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Summary1. The noradrenaline (NA) concentration in the "heart" (atria and right ventricle) of male rats was estimated at different periods following adrenal demedullation. For 1-3 weeks after the operation there was, in all rats, a reduction in NA content of the tissue, whereas, after somewhat longer intervals, the concentrations had returned to normal in some but not in all animals, so that the range of values was very wide. 2. In order to be able to test the effect of 2-aminotetralin on the cardiac NA of animals deprived of their medulla but having normal initial NA concentrations, an interval of 6-8 months was allowed to elapse between operation and injection of the drug; at this time the effect of the drug on cardiac NA was the same in intact and demedullated animals. There is thus no reason to attribute to the adrenal medulla any supporting role in the resynthesis of cardiac NA during periods of increased sympathetic activity. 3. The time course of the pronounced fall in cardiac NA after adrenal demedullation resembles the time course of sodium retention shown by Gaunt, Renzi, Gisoldi & Howie (1967) to follow this operation. It is therefore suggested that it is the change in electrolyte metabolism which is responsible for the abnormality of NA storage; both phenomena occur in demedullated but not in adrenalectomized animals.

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Section: Discussionsupporting

confidence: 51%

supporting

confidence: 63%

Section: Discussionmentioning

confidence: 97%

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Noradrenaline content of the heart of the adrenal‐demedullated rat

Borchard

Vogt

1970

British J Pharmacology

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“…It is possible that the transient increase in proliferation results, in part, from stimulation by angiotensin II, a primary stimulus for in vivo growth of glomerulosa cells in rats (25). Plasma angiotensin has not been measured after enucleation, but increased sodium retention occurs during the first week of regeneration (14). Enhanced sodium retention is a critical element in the development of adrenal regeneration hypertension after enucleation, which is exacerbated by unilateral nephrectomy and increased salt intake (34).…”

Section: Discussionmentioning

confidence: 99%

Zone-specific cell proliferation during adrenocortical regeneration after enucleation in rats

Ennen¹,

Levay‐Young²,

Engeland³

2005

American Journal of Physiology-Endocrinology and Metabolism

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A quantitative analysis of zone-specific proliferation was done to determine the recovery of adrenal cortical zonation during regeneration after enucleation. Adult male rats underwent adrenal enucleation [unilateral enucleation (ULE)] or sham surgery, both accompanied by contralateral adrenalectomy. At 2, 5, 10, and 28 days, blood and adrenals were collected to assess functional recovery. Adrenal sections were immunostained for Ki67 (proliferation), cytochrome P-450 aldosterone synthase (P-450aldo, glomerulosa), and cytochrome P-450 11beta-hydroxylase (P-45011beta, fasciculata). Unbiased stereology was used to count proliferating glomerulosa and fasciculata cells. Recovery of fasciculata secretory function occurred by 28 days as reflected by plasma ACTH and corticosterone, whereas glomerulosa function reflected by plasma aldosterone remained low at 28 days. At 5 days, ULE adrenals showed increased Ki67+ cells in the glomerulosa and inner fasciculata, whereas at 10 and 28 days increased proliferation was restricted to the outer fasciculata. These data show that enucleation results in transient elevations in glomerulosa and inner fasciculata cell proliferation followed by a delayed increase in the outer fasciculata. To assess adrenal growth in enucleated adrenals previously suppressed by the presence of an intact adrenal, rats underwent ULE and sham surgery; after 4 wk, the intact adrenal was removed and enucleated adrenals were collected at 2, 5, and 10 days. Overall, proliferation was delayed in this model, but at 5 days, Ki67+ cells increased in the outer fasciculata, whereas by 10 days, increased proliferation occurred in the outer and inner fasciculata. The key novel finding of increased proliferation in the inner fasciculata suggests that the delayed growth of the enucleated adrenal results in part from a regenerative response.

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