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James A. Haley Veterans Hospital Tampa, Florida 33612
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.
Normal renal kaliuretic effect of the potassium load and fludrocortisone in the subjects with GRA suggests that the renal responsiveness to potassium and to mineralocorticoid probably is unimpaired. Plasma aldosterone levels in the two groups, however, were different. The increased urinary potassium excretion by the kidney under the influence of aldosterone is coupled with enhanced sodium reabsorption through the sodium channels and activation of Na-K-ATPase in the renal cortical collecting tubule. This relationship of sodium absorption and potassium excretion is not stoichiometric, but it is influenced by a complex interplay of serum potassium level, plasma aldosterone level, and sodium delivery to the appropriate renal tubules (11). Aldosterone-induced proton secretion is not coupled to potassium loss or sodium absorption. If a lesser degree of elevation of plasma aldosterone level (as compared with primary aldosteronism) is the determinant of the normokalemia in GRA, then a difference in the renal responsiveness between GRA subjects and normal subjects or subjects with primary aldosteronism cannot be completely excluded from this study because of the differing baseline plasma aldosterone levels between the two groups studied. The magnitude of the hypertension in GRA subjects, if compared with that in subjects with primary aldosteronism, may also be of interest in the perspective of plasma aldosterone and potassium levels.
Finally, there is an oversight in the reference of the paper. The authors meant to refer to our paper in the New England Journal of Medicine dealing with GRA patients and not the one referred to (reference no. 22) in their article in the appropriate context.
Footnotes
Received June 2, 1997. Address correspondence to: Arunabha Ganguly, Research Service (151), Building 2, Room 208, J. A. Haley Veterans Hospital, 13000 Bruce B. Downs Boulevard, Tampa, Florida 33612.
References
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