Figure 3.

Pathophysiologic renin-independent aldosteronism in primary aldosteronism. The primary problem is that one or both adrenal glands contain foci of autonomous aldosterone secretion. There is increased stimulation of the MR in principal cells, despite the fact that circulating volume is expanded and renin and angiotensin II are suppressed. This results in increased and inappropriate sodium reabsorption as well as a vicious cycle of further volume expansion and greater distal delivery of sodium. Because potassium and hydrogen ion excretion are paired with sodium reabsorption in the principal cell, these processes are also increased. The net effect is volume expansion, increases in blood pressure, hypokalemia, and metabolic alkalosis. AngII, angiotensin II. [© 2018 Illustration ENDOCRINE SOCIETY]