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Arunabha Ganguly, Potassium and Aldosterone Secretion in Glucocorticoid-Remediable Aldosteronisme, The Journal of Clinical Endocrinology & Metabolism, Volume 82, Issue 12, 1 December 1997, Pages 4276–4277, https://doi.org/10.1210/jcem.82.12.4466-5
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The results of potassium administration on plasma aldosterone concentration in the studies involving patients with glucocorticoid-remediable aldosteronism (GRA) by Litchfield et al. (1) in the May issue of The Journal of Endocrinology and Metabolism are interesting. It is likely that the aldosterone response to potassium reported in these patients reflects different cellular characteristics of the aldosterone-producing cells in such patients compared with those in the normal subjects. This blunted aldosterone response to potassium may also be true to some degree (2) in patients with aldosteronoma (of the angiotensin-unresponsive variety), and that also may be related to the cell origin or cell characteristics of these aldosteronomas, cells of which may share some of the features with the aldosterone-producing cells of GRA (3). Alternatively, the response in these subjects could be related to the lack of the permissive effect of angiotensin II for the potassium-mediated stimulation of aldosterone secretion (4).
The belief that the source of excessive aldosterone secretion in GRA is the fasciculata cells harboring an abnormal steroidogenic enzyme gene (5) may explain the aberrant aldosterone response to potassium. It has been established now that steroid secretion from the fasciculata cells generally is not modulated by potassium, even when similar electrophysiological effects are produced by potassium in the fasciculata and the glomerulosa cells (6), although there can be steroid response from the fasciculata cells to potassium in some species (7). As discussed, the discordance between the electrophysiological and the steroid responses to potassium in the fasciculata cells might be related to a qualitative or a quantitative difference in calcium channels between the two types of adrenal cells (8). As a result perhaps, elevation of cytosolic free calcium concentration in response to potassium (usual concomitant of aldosterone response to potassium in the glomerulosa cells) has not been observed to occur in the rat fasciculata cells (9). Thus, at least in the rat, the fasciculata cells appear to lack the cellular signaling mechanism necessary for stimulation of aldosterone secretion by the increment of extracellular potassium. This could also be true in the human. This failure of potassium to enhance aldosterone secretion in GRA seems to confirm that the fasciculata cells are indeed the source of excessive aldosterone secretion in this disorder, provided the stimulating effect of potassium was not blunted (10) by the calcium channel blocker some of the subjects received.
