Aim of the study was to evaluate the influence of nifedipine on the proximal tubular handling of sodium, as judged by variations in the fractional excretion of lithium, which is a simple and reliable indicator of sodium and water reabsorption at this site. Lithium clearance was determined in 17 in-hospital essential hypertensives who took 16 mmol of lithium per os at 10 p.m. The following morning, urine was collected from 7 to 11 a.m. to determine sodium, potassium, lithium and creatinine concentration. The same analyses were performed in a sample of venous blood drawn at midpoint of the urine collection (9 a.m.). The test took place in basal conditions and was repeated 48 hours later when the patients assumed nifedipine, 10 mg per os, at the beginning of the urine collection (7 a.m.). Compared to basal values, nifedipine increased urinary sodium excretion (mean basal: 33.65 +/- 19.44 mEq/4 h; after nifedipine: 46.99 +/- 19.22) with no change in the fractional excretion of lithium. We conclude that the acute natriuretic effect of this calcium antagonist does not depend on variations in proximal tubular handling of sodium.