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In a relatively brief article it is not possible to fo cus in detail on all aspects o f this topic, and we have referred to key reviews where possible.

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J Endocrinol 186:1-20 August 2005 Journal of Endocrinology 186(1):1-20 DOI: 10.1677joe.1.06017 Source PubMed Authors: John Connell Central New Mexico Community College Eleanor May Davies Oxford Brookes University Download full-text PDF Read full-text Download full-text PDF Read full-text Download citation Copy link Link copied Read full-text Download citation Copy link Link copied Citations (218) References (209) Abstract 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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Translocatio n of the resulting stero id receptor co mplex to the cell nucleus modulates gene expressio n and translation of specic aldostero ne-induced proteins that regulate electrolyte and uid balance.

Ho wever, non-epithelial and rapid non-geno mic actions o f aldosterone have also been described that account fo r a variety of actio ns of aldosterone that co ntribute to bloo d pressure homeostasis.

These include key actions o n endothelial cells and o n cardiac tissue.

There is also evidence that aldosterone can be syn- thesised in other tissues; the most co nvincing evidence relates to the central nervous system.

Ho wever, sug- gestions that aldostero ne is produced in the heart remain contro versial, and adrenal derived aldosterone is the principal source o f circulating and locally available hormo ne.

Additional evidence demo nstrates that aldosterone levels predict development o f high bloo d pressure in normo- tensive subjects, while it is now clear that increased aldosterone actio n contributes to hypertensio n and cardio- vascular damage in approximately 10 o f patients with established hypertension.

These new ndings highlight the role o f aldosterone as a key cardiovascular ho rmone and extend o ur understand- ing of its ro le in determining adverse cardiovascular outco mes.

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Journal of Endocrinology (2005) 186, 120 Introductio n It is now o ver 50 years since Sylvia and James Tait, in collabo ration with Tadeusz Reichstein, iso lated and characterized the steroid ho rmone, aldostero ne (Tait et al.

Since then, the traditional view has been that the hormo ne is synthesized in the adrenal gland and binds to specic mineraloco rticoid recepto rs (MRs) located in the cytosol o f target epithelial cells.

This steroid recepto r com- plex then translocates to the cell nucleus where it mo dulates gene expression and translatio n of specic aldostero ne- induced proteins that regulate electro lye and uid balance and subsequent bloo d-pressure homo eostasis.

However, a number of recent studies sho w that aldosterone also has marked e ects in a wide range of no n-epithelial tissues (such as the heart), that it can be synthesized and regulated in a number of extra-adrenal tissues and that it may act through alternative recepto rs in epithelial and non- epithelial tissue in a rapid non-geno mic manner which is independent of gene transcriptio n and translation.

Recently, there has been a new wave of interest in aldosterone due mainly to its gro wing prole as a key cardiovascular ho rmone.

The impo rtance of aldostero ne in cardiovascular ho moeostasis is evident in animal models where expressio n of co mponents o f the aldosterone biosynthetic pathway or o f mineraloco rticoid actio n is abolished o r increased, and in the rare human mono genic syndromes that result in either an absence o r an excess of aldosterone.

Recent wo rk now sho ws that aldosterone levels within the upper part of the physio logical range predispose normo tensive subjects to the development o f hypertension and that majo r therapeutic benets result from MR antago nism in cardiac failure (Vasan et al.

In this review we outline so me of the recent advances in our kno wledge of aldostero ne biosynthesis, its novel sites of actio n and the mechanism and specicity of this actio n.

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