Figure:

Schematic representation of the mechanisms of autonomous aldosterone production in primary hypertension. Aldosterone production from the adrenal zona glomerulosa is independent of the renin-angiotensin system and is not suppressible with dietary sodium loading. Excess aldosterone expands extracellular fluid volume by augmenting sodium reabsorption in the renal cortical collecting duct. Expanded fluid volume leads to hypertension and suppression of renin and the entire renin-angiotensin cascade. Increased aldosterone production is abnormal in the face of renin suppression but plasma aldosterone concentrations are lower than those of patients with classical overt primary aldosteronism. ACE, angiotensin converting enzyme; Ang, angiotensin; AT₁, angiotensin type-1. Dashed line and grey tone indicates suppression.