Abstract

Aldosterone, the most potent naturally occurring mineralocorticoid, plays a major role in regulation of the amounts of both sodium and potassium in the body. The hormone acts on the kidney tubules to increase both sodium reabsorption and the secretion of potassium ions. Because of these two simultaneous actions, there would appear to be a conflict of interest in constructing a homeostatic regulatory system for the simultaneous maintenance of the balance of the two cations, sodium and potassium, by this one hormone. Because of the two concurrent actions of aldosterone, one might expect that changes in its activity would inevitably accomplish defense in the balance of one ion at the expense of the other. One might expect, for example, that increases in aldosterone secretion in response to sodium depletion would, while defending, sodium balance, also produce potassium loss or, conversely, that after potassium ingestion the induced increase in aldosterone secretion would, in the course of promoting kaliuresis, cause unwanted sodium retention. Obviously, neither happens. In fact sodium balance remains stable in the face of wide changes in potassium intake and vice versa. This analysis is concerned then with the question of how the kidney adjusts to variations in both sodium and potassium intake to compensate for the two concurrent actions of aldosterone and to enable the appropriate excretion of both cations. In particular, the presentation considers how changes in sodium and potassium intake affect intrarenal physical factors and how, in turn, these intrarenal changes are coordinated with changes in aldosterone secretion to compose a balanced control system which works to stabilize the balance of one cation while reacting to wide fluctuations in intake of the other. First, the hormonal responses to changes in sodium and potassium intake will be characterized. Then, an analysis of the simultaneous and complementary changes in intrarenal physical factors will be presented.

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