Aldosterone secretion and the mechanism of potassium adaptation in rats

Abstract

In order to better understand the cellular mechanism of potassium (K + adaptation, the sensitivity of aldosterone secretion to acute changes in extracellular K + concentration was studied in freshly dissected adrenal capsules of rats adapted to diets of high or low K + content, of rats adapted to low or high sodium (Na +) diets, and also of control rats. in control tissues, the aldosterone secretion from the capsules of an individual animal averages 0.44 ± 0.05 nmol/h, increasing 4.4-fold between 2 and 8 mM K + but decreasing between 8 and 10 mM K +. Although a high K + diet increases aldosterone secretion by only 34% at 4 mM K +, the rate of secretion increases 3.7-fold more steeply than control as the K + concentration increases. This change is equivalent to a parallel 3.1-fold increase in the effective number of T- and L-type calcium (Ca 2+) channels, accompanied by a 1.3-fold increase in the K +-insensitive rate of aldosterone secretion. In contrast, after Na + restriction, aldosterone secretion is about 3 times the control rate for all K + concentrations tested, equivalent to an increase in the basal rate and the effective number of L-channels. Thus, the alteration in the number of effective T-channels is specific to diets of increased K + content, not simply an effect of increased secretory capacity. After a low K + diet, aldosterone secretion is 18% of control at 4 mM K + and changes little with the K + concentration, consistent with a 94% to 96% decrease in the effective number of T- and L-channels plus a 77% decrease in the K +-insensitive rate of aldosterone secretion. Similarly, the rate of aldosterone secretion is reduced and shows little sensitivity to changes in extracellular K + after Na + repletion. These changes in K + sensitivity are sufficient to explain the altered serum aldosterone concentrations observed after the high K + and Na + diets and the low K + diet ( r = 0.9); however, serum aldosterone is threefold greater than predicted for the low Na + diet, consistent with the dominance of angiotensin II stimulation during Na + depletion. In conclusion, adaptations to changes in dietary potassium are primarily due to altering the magnitude of the response to a change in extracellular K + concentration and are apparently mediated by T- and L-type Ca 2+ channels.