Abstract

Article, see p 347 The study by Nanba et al, “Age-related autonomous aldosteronism,”1 in this issue of Circulation , addresses 2 areas of current major interest in cardiovascular endocrinology. The first is that of aldosterone-producing cell clusters (APCCs), distinct from a more or less continuous outer layer of aldosterone-producing cells familiar as the zona glomerulosa of the adrenal gland. The second is that of the changes in plasma renin activity (PRA) and serum aldosterone concentration with age in a group of normotensive and stage 1 hypertensive patients from the HyperPATH study (Hypertensive Pathotype), with primary aldosteronism based on current criteria excluded. The study is novel in terms not only of the numbers involved (adrenal glands from kidney donors n=127, HyperPATH cohort n=677), but also in the possibilities of linking the 2 lines of study into a coherent explanation of the changes seen in human aging. The presentation is also straightforward, crisp, and clear, with the discussion, in particular, mercifully free of padding and nit-picking: for this, and the novelty and possible implications of their findings, as well, we owe the authors our thanks. What the study shows is that there are 2 apparently related changes in aldosterone secretion with age. In adrenal glands from young organ donors, the zona glomerulosa appears as a thin continuous outer layer, as identified by immunohistochemistry with antibody specific for the enzyme aldosterone synthase (CYP11B2). When adrenal glands from older donors are examined, the previously continuous zona glomerulosa appears disrupted (or discontinuous), progressively with increasing age. At the same time, isolated aldosterone-producing cell clusters appear more and more commonly. Whereas the factors controlling aldosterone secretion from zona glomerulosa cells are well established, those from APCCs are not; on the basis that secretion from APCCs may be constitutive, the authors suggest that this may represent …

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