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Ying-Ying Tsai, William E Rainey, and Wendy B Bollag

Aldosterone, secreted by the adrenal zona glomerulosa, enhances sodium retention, thus increasing blood volume and pressure. Excessive production of aldosterone results in high blood pressure and contributes to cardiovascular and renal disease, stroke and visual loss. Hypertension is also associated with obesity, which is correlated with other serious health risks as well. Although weight gain is associated with increased blood pressure, the mechanism by which excess fat deposits increase blood pressure remains unclear. Several studies have suggested that aldosterone levels are elevated with obesity and may represent a link between obesity and hypertension. In addition to hypertension, obese patients typically have dyslipidemia, including elevated serum levels of very low-density lipoprotein (VLDL). VLDL, which functions to transport triglycerides from the liver to peripheral tissues, has been demonstrated to stimulate aldosterone production. Recent studies suggest that the signaling pathways activated by VLDL are similar to those utilized by AngII. Thus, VLDL increases cytosolic calcium levels and stimulates phospholipase D (PLD) activity to result in the induction of steroidogenic acute regulatory (StAR) protein and aldosterone synthase (CYP11B2) expression. These effects seem to be mediated by the ability of VLDL to increase the phosphorylation (activation) of their regulatory transcription factors, such as the cAMP response element-binding (CREB) protein family of transcription factors. Thus, research into the pathways by which VLDL stimulates aldosterone production may identify novel targets for the development of therapies for the treatment of hypertension, particularly those associated with obesity, and other aldosterone-modulated pathologies.

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Renaud Beauwens, Marion Birmingham, and Jean Crabbé

The effects on sodium transport of several steroids physiologically secreted or possibly involved in pathological disorders were compared with those of aldosterone in the isolated toad skin.

The 18-hydroxylated derivatives of deoxycorticosterone and corticosterone, in contrast to their parent compounds, significantly enhanced sodium transport at a concentration of 50 nmol/l. In the presence of glucose, 18-hydroxydeoxycorticosterone increased trans-epithelial potential difference, as did aldosterone. The 19-nor derivative of deoxycorticosterone, recently implicated in the aetiology of adrenal regeneration hypertension, stimulated sodium transport, unlike 19-nor-corticosterone and 16-oxo-androstenediol. Insulin significantly increased sodium transport in aldosterone-treated skin and lowered the resistance. The natriferic response to vasopressin was potentiated fivefold by exposure of the skin to aldosterone and was doubled in skin exposed to 19-nor-deoxycorticosterone.

We conclude that 18-hydroxylated adrenocortical steroids can play a physiological role in salt retention; furthermore, these steroids, as well as 19-nor-deoxycorticosterone, could be involved in pathological conditions such as low renin hypertension. Caution should be exercised in evaluating mineralocorticoid potency solely in terms of the urinary sodium to potassium ratio.

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Kelly De Sousa, Alaa B Abdellatif, Rami M El Zein, and Maria-Christina Zennaro

Primary aldosteronism (PA) is the most common form and an under-diagnosed cause of secondary arterial hypertension, accounting for up to 10% of hypertensive cases and associated to increased cardiovascular risk. PA is caused by autonomous overproduction of aldosterone by the adrenal cortex. It is mainly caused by a unilateral aldosterone-producing adenoma (APA) or bilateral adrenal hyperplasia. Excess aldosterone leads to arterial hypertension with suppressed renin, frequently associated to hypokalemia. Mutations in genes coding for ion channels and ATPases have been identified in APA, explaining the pathophysiology of increased aldosterone production. Different inherited genetic abnormalities led to the distinction of four forms of familial hyperaldosteronism (type I to IV) and other genetic defects very likely remain to be identified. Somatic mutations are identified in APA, but also in aldosterone-producing cell clusters (APCCs) in normal adrenals, in image-negative unilateral hyperplasia, in transitional lesions and in APCC from adrenals with bilateral adrenal hyperplasia (BAH). Whether these structures are precursors of APA or whether somatic mutations occur in a proliferative adrenal cortex, is still a matter of debate. This review will summarize our knowledge on the molecular mechanisms responsible for PA and the recent discovery of new genes related to early-onset and familial forms of the disease. We will also address new issues concerning genomic and proteomic changes in adrenals with APA and discuss adrenal pathophysiology in relation to aldosterone-producing structures in the adrenal cortex.

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A case is described in which the presence of an adrenal cortical adenoma was predicted from the association of hypertension, hypokalaemia, raised aldosterone secretion and depressed plasma renin concentration.

Pre-operatively, administration of a spironolactone for a period of 10½ months corrected the electrolyte abnormalities, increased the plasma renin concentration to normal and lowered the blood pressure, although the raised aldosterone secretion was unchanged.

At operation a typical adrenal cortical adenoma was found.

Renal biopsy at operation showed arteriolar fibrinoid lesions, although no retinal lesions were seen at any stage.

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1. The characteristic response of the autotransplanted adrenal gland of the sheep to sodium depletion was an increase in aldosterone secretion rate, which reached the minimum detectable level of 1 μg/hr 6–12 hr after the Na balance became negative, when the Na deficit was approx. 200 m-equiv.

2. After its initial detection, aldosterone secretion altered in an irregular manner to maximum secretion rates of 5–9 μg/hr.

3. The initial detection of aldosterone secretion was not accompanied by any consistent changes in cortisol and corticosterone secretion.

4. Changes in cortisol and corticosterone secretion rates were usually in the same direction and of similar relative magnitude, and did not show any consistent correlation with the aldosterone secretion rates. The rates of cortisol and corticosterone secretion were extremely variable, but there was inconclusive evidence that there may have been a natural periodic variation of secretion rate, characteristic for individual sheep, which was modified by the experimental procedure.

5. The relationship between adrenal corticosteroid secretion and changes in blood plasma and urine electrolytes as well as haematocrit, plasma protein concentration and adrenal blood flow was examined.

6. Attention is drawn to the possible complexity of the relationship between adrenal corticosteroid secretion and the salivary Na/K ratio.

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John M C Connell and Eleanor Davies

Classically, aldosterone is synthesised in the adrenal zona glomerulosa and binds to specific mineralocorticoid receptors located in the cytosol of target epithelial cells. Translocation of the resulting steroid receptor complex to the cell nucleus modulates gene expression and translation of specific ‘aldosterone-induced’ proteins that regulate electrolyte and fluid balance. However, non-epithelial and rapid non-genomic actions of aldosterone have also been described that account for a variety of actions of aldosterone that contribute to blood pressure homeostasis. These include key actions on endothelial cells and on cardiac tissue.

There is also evidence that aldosterone can be synthesised in other tissues; the most convincing evidence relates to the central nervous system. However, suggestions that aldosterone is produced in the heart remain controversial, and adrenal derived aldosterone is the principal source of circulating and locally available hormone.

Recent studies have shown major therapeutic benefits of mineralocorticoid receptor antagonism in cardiac failure, which emphasise the importance of aldosterone in causing adverse cardiovascular pathophysiological effects. Additional evidence demonstrates that aldosterone levels predict development of high blood pressure in normotensive subjects, while it is now clear that increased aldosterone action contributes to hypertension and cardiovascular damage in approximately 10% of patients with established hypertension.

These new findings highlight the role of aldosterone as a key cardiovascular hormone and extend our understanding of its role in determining adverse cardiovascular outcomes.

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M. Haji, Y. Nishi, S. Tanaka, M. Ohashi, K. Sekiya, Y. Hasegawa, M. Igarashi, S. Sasamoto, and H. Nawata


We have studied the production and release of inhibin-like immunoreactivity in the human adrenal gland. Extract of human adrenal glands showed a displacement curve paralled with the inhibin standard. Inhibin-like immunoreactivity contents in the adrenal gland was 1893±474 (mean±S.D.) IU/g wet weight tissue. ACTH stimulated the secretion of inhibin-like immunoreactivity as well as cortisol and aldosterone in a dose-dependent manner in the cultured adrenal cells. These results indicate that the human adrenal gland produces and secretes inhibin-like peptide in response to ACTH.

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Comparisons of aldosterone responses to [des-Asp1]-angiotensin II and angiotensin II, often at single dose levels, have shown a wide range of potency ratios. Therefore four-point dose–response comparisons were performed in sodium-replete sheep, using i.v. infusion rates of angiotension II and angiotensin II amide that reproduced the physiological range of blood concentration of angiotensin II for sheep. Angiotensin III was infused i.v. at the same rates. Effects on arterial blood pressure, cortisol secretion rate, adrenal blood flow and plasma levels of Na+ and K+ were also compared. The potency ratio, angiotensin III: angiotensin II amide, was 0·87 for actual aldosterone secretion rate and 0·90 for the calculated increase in aldosterone secretion. For angiotensin III: angiotensin II the ratios were 0·80 and 0·91 respectively. These ratios were not significantly different from 1·00 but the tendency for angiotensin II to be slightly more potent was probably due to a contribution from derived angiotensin III during infusion of angiotensin II. Angiotensin II or angiotensin II amide was ∼ four times as potent as angiotensin III in raising arterial blood pressure. Cortisol secretion rate was slightly but significantly increased by all peptides at the higher infusion rates. Infusions had no effect on adrenal blood flow or plasma levels of Na + but raised plasma levels of K + slightly. These results confirm the conclusion from adrenal arterial infusion experiments that angiotensin II and III are almost equipotent in stimulating aldosterone secretion in sheep.

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In hypophysectomized-nephrectomized dogs after intravenous injection of histamine, a marked increase was observed in the rate of secretion of aldosterone, although it was smaller than that in intact dogs. Hypophysectomy plus bilateral nephrectomy greatly impaired the secretion of corticosterone and cortisol in the dog in response to histamine. However, a small yet significant increase in corticosterone and cortisol secretion was observed in hypophysectomized-nephrectomized dogs after intravenous injection of histamine. Additional experiments showed that plasma concentrations of potassium and sodium in hypophysectomized-nephrectomized dogs remained unchanged after intravenous injection of histamine. These results suggest that histamine stimulates aldosterone secretion in the dog partly by a direct effect on the adrenal cortical cells, whereas the effect of histamine on corticosterone and cortisol secretion is mediated mainly, but not totally, by pituitary release of ACTH.

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1. No alteration in cerebral water content was observed in rats following administration of cortisol, aldosterone or the adrenal inhibitor 2 methyl-1,2-di-3′ pyridylpropan-1-one (SU 4885).

2. Aldosterone was found to decrease the cerebral oedema produced by intravenous injection of water.

3. Cortisol and SU 4885 had no effect on cerebral water content following intravenous administration of water.