Nifedipine-induced kidney dopamine production in hypertensive patients. Double-blind placebo controlled study

Dopamine is synthesized and excreted by kidneys, this amine exerts its natriuretic and diuretic effects by inhibition of sodium reabsorption on kidney convoluted tubules. The objective of this study was to verify the changes of dopamine urinary excretion induced by nifedipine-LP treatment in hypertensive patients. Twenty four patients with essential hypertension (stages 1, 2) were included in this double-blind, placebo controlled study. Twelve patients received nifedipine (average daily dose, 21.5 mg/day) for 4 weeks, and 12 patients received placebo for the same time period. No significant changes were detected upon nifedipine treatment neither in plasma biochemical nor hematological parameters. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) was significantly reduced from pretreatment values 168.0 ± 8.7 mmHg and 102.0 ± 5.2 mmHg respectively, to end-treatment values values 140.0 ± 6.6 mmHg and 88.0 ± 5.6 mmHg (p < 0.05). Placebo treatment did not modify SBP and DBP. Urinary dopamine excretion increased by 53% from 679.5 ± 80.1 μg/24 h prior to treatment to 1040.0 ± 110.1 μg/24 h after treatment (p < 0.009. 95% Confidence Interval of the Difference: -538.9 to -183.6). Urinary volume of nifedipine treated patients increased from 1613 ± 85 mL/24 h to 1920 ± 160 mL/24 h post-treatment (p < 0.05). No significant changes were observed in urinary noradrenaline and adrenaline excretion in nifedipine or placebo treated patients. Analysis of fluorescent light excitation and emission spectra (200 nm to 800 nm) of dopamine extracted from patient's urine submitted to nifedipine treatment did not reveal any interference when compared to chemically pure dopamine. It is concluded that nifedipine treatment of hypertensive patients increases kidney dopamine production which in turn can exert a natriuretic and diuretic effect besides its well known vasodilator properties.