Enhanced renal vasoconstriction and renal tubular sodium reabsorption mediated by noradrenaline and angiotensin II (Ang II) have been implicated in the pathogenesis of essential hypertension. Since these effects seem to be calcium-dependent, renal haemodynamic and tubular function were studied following acute and long-term treatment with the calcium antagonist felodipine in 10 patients with essential hypertension.After acute felodipine administration mean blood pressure (MBP) decreased (from 111 to 95 mmHg;P< 0.01), renal blood flow (RBF), estimated from hippurate clearance, increased (from 1030 to 1175ml/min;P< 0.01) and glomerular filtration rate (GFR) was unchanged (109 versus 112ml/min). Fractional excretion (FE) of sodium, potassium, calcium, magnesium, chloride, bicarbonate and urate increased for 12 h. Following long-term felodipine treatment, mean blood pressure was reduced (97 mmHg;P< 0.01) and RBF and GFR were unchanged (1032 and 114ml/min, respectively). Fractional excretion of urate and calcium was increased for 24 h (from 5.9 to 6.9%;P< 0.05 and from 1.1 to 1.3%;P< 0.05, respectively). Serum urate decreased (from 377 to 347 µmol/l;P< 0.01) whereas serum calcium was unchanged. Fractional excretion of sodium, potassium and chloride was increased between 3 and 6 h after felodipineThe renal haemodynamic findings after acute felodipine administration are indicative of a direct renal vasodilator action of felodipine which augments the autoregulatory renal vasodilation to produce an overall increase in RBF. Since GFR was unchanged, the increased renal excretion of electrolytes and urate reflects an action at the tubular level. Following long-term felodipine administration autoregulatory adjustment of RBF predominated