We previously observed that, in subjects with essential hypertension, acute ouabain constricts the brachial artery diameter in the presence of spironolactone treatment, a finding that is not observed in the absence of aldosterone antagonist and therefore suggests a specific effect of aldosterone on the arterial wall. To evaluate whether aldosterone excess may contribute to modulate arterial function, we investigated 56 patients with sustained essential hypertension in comparison with 36 normotensive controls. Systemic arterial compliance was measured from intraarterial blood pressure and cardiac output measurements using a classical Windkessel model to determine the elasticity of the proximal arterial tree. Radial artery compliance was determined using a previously described echo tracking technique. In hypertensive, but not in normotensive, subjects, systemic arterial compliance was strongly and negatively correlated with plasma aldosterone. The correlation was observed even after adjustment for age and blood pressure. Plasma potassium and renin activity did not interfere in the correlation. Acute administration of diltiazem did not change systemic compliance but significantly decreased plasma aldosterone, suggesting that, in the presence of calcium blockade, the same compliance was achieved for a lower plasma aldosterone level. Taken together, these findings strongly suggest that significant interactions exist between aldosterone and central conduit arteries and that aldosterone might modulate arterial function in subjects with essential hypertension.