Aldosterone and potassium homeostasis

Abstract

The presently accepted regulators of the homeostatic excretion of potassium are the plasma concentrations of aldosterone and potassium. Evidence for a role of aldosterone is reviewed, and it is pointed out that aldosterone is kaliuretic at supraphysiologic levels but has little kaliuretic activity within its normal secretory range. Elevation of plasma potassium above its normal range enhances the kaliuretic action of aldosterone. Elevation of plasma potassium above, but not within, its normal range is strongly kaliuretic. In sheep the kaliuresis induced by intake of a potassium rich meal cannot be explained by changes in aldosterone or plasma potassium. A kaliuretic reflex arising from receptors in the gut, portal vein or liver has been proposed the explain the meal-induced kaliuresis. This putative reflex involves the central nervous system and efferent kaliuretic factors other than aldosterone and plasma potassium. Evidence for the involvement of the central nervous system and undetermined kaliuretic regulatory factors can be found in studies of the physiologic circadian rhythm of renal potassium excretion. This rhythmic excretion does not appear to depend on changes in either aldosterone or plasma potassium.

The mislabelling of deoxycorticosterone: making sense of corticosteroid structure and function

“…As an addendum, it is interesting to note that the actions even of aldosterone on potassium excretion are not necessarily physiological, and though its role may once have been considered crucial, other mechanisms for potassium regulation must now be considered relevant (Rabinowitz 1996, Greenlee et al 2009). …”

Gut sensing of dietary K+ intake increases renal K+ excretion

“…Thus, the maintenance of K ϩ homeostasis has been traditionally understood on the basis of the concept of negative feedback control. However, Rabinowitz (21,22) challenged this traditional view when he pointed out that plasma K ϩ and aldosterone can stimulate renal K ϩ excretion only at levels above their normal ranges (3,25,31,32). In his studies in the sheep (24), meal intake over 1 h produced a pronounced kaliuresis, which occurred in the absence of a change in plasma aldosterone concentration and with only a very small (0.5 meq/l) increase in plasma [K ϩ ].…”

“…Extracellular [K ϩ ] increases during dietary K ϩ intake, and this increase then stimulates renal K ϩ excretion by increasing K ϩ secretion in the collecting duct directly (11,30) and indirectly by stimulating aldosterone secretion (21,22). Increased renal K ϩ excretion then normalizes extracellular [K ϩ ].…”

Mechanisms of Renal Control of Potassium Homeostasis in Complete Aldosterone Deficiency

“…17 Nevertheless, despite these clinical observations and numerous experimental studies confirming the relevance of aldosterone, it becomes increasingly clear that regulation of K + homeostasis is at least in part also independent from aldosterone. [18][19][20] Indeed, the kaliuretic response to a dietary K + load occurs very rapidly and often before plasma aldosterone is elevated. 18 Moreover, even in adrenalectomized animals, increased K + intake augments K + excretion in kidney and colon.…”

“…[18][19][20] Indeed, the kaliuretic response to a dietary K + load occurs very rapidly and often before plasma aldosterone is elevated. 18 Moreover, even in adrenalectomized animals, increased K + intake augments K + excretion in kidney and colon. 3,21 Likewise, dietary K + increases apical Na + and K + channel conductances in the CD not only of intact but also of adrenalectomized rats 19,21 and rabbits.…”