Figure 1. Diagram illustrates the renin-angiotensin-aldosterone axis. Physiologic release of aldosterone occurs if there is a reduction in the effective circulating volume (eg, hemorrhage). Aldosterone works by increasing sodium retention in the distal renal tubules, which in turn promotes water absorption and causes isotonic expansion of the effective circulating volume. Aldosterone is also a potent vasoconstrictor. Both of these mechanisms serve to increase blood pressure (BP). This increase is detected by cells of the juxtaglomerular apparatus, which suppress renin production as part of a negative feedback mechanism. In primary aldosteronism, this negative feedback mechanism is overridden by the pathologic excess of aldosterone, which occurs in the absence of an appropriate stimulus.