Natriuretic effect of nitrendipine is preceded by transient systemic and renal hemodynamic effects.

This study investigated whether the acute natriuretic effect of nitrendipine is related to its initial renal hemodynamic effects. We investigated 16 patients (10 men and 6 women, mean age 52 +/- 2 years) with essential hypertension, whose treatment, if any, was stopped 3 weeks before the study. They were admitted to a metabolic ward for 9 days and kept on a constant sodium diet of 55 mmol/day. During two 24-hour experiments, subjects randomly received a single oral dose of placebo/nitrendipine 10 mg (group 1, n = 8) or placebo/nitrendipine 20 mg (group 2, n = 8), according to a double-blind crossover study design. Patients fasted during the experiments, but their sodium intake was ensured by a constant intravenous saline infusion of 2.3 mmol/hr. Mean arterial pressure (MAP) and heart rate were determined for 5 hours following the administration of nitrendipine or placebo. Effective renal plasma flow (ERPF), glomerular filtration rate, active plasma renin concentration, angiotensin II, aldosterone, atrial natriuretic peptide, and catecholamines were determined every hour for 5 hours. Hourly urine collections were used to assess sodium, potassium, and creatinine excretions. Relative to placebo, only in group 2 (nitrendipine 20 mg) was a fall in MAP and a rise in ERPF observed 2 hours after the start of the experiment. The effects, however, lasted only for 1 hour. No such changes were seen in group 1. In neither group did nitrendipine affect hormonal concentrations. Sodium excretion was enhanced after the 20-mg dose of nitrendipine only (p < 0.05). Nitrendipine 20 mg induced a significant increase in sodium excretion, which may be dissociated from its acute hemodynamic effects.