Catecholamine Excretion in ‘Idiopathic’ Edema: Decreased Dopamine Excretion, a Pathogenic Factor?

Abstract
In 16 women with idiopathic edema, urinary dopamine excretion was decreased when compared to control women (146± 13 SE ng/ml/m2vs. 212± 32, P < 0.05 in the supine position and 140± 9 vs. 199± 20, P < 0.005 combined values of supine and recumbent positions) and was also lower when pooled values for urinary dopamine excretions both before and after furosemide were compared in idiopathic edema patients and in control subjects (270± 30 ng/ml vs. 480±70, P < 0.05). These patients have lower basal sodium excretions, decreased tubular rejection fractions of sodium in the upright position and lower urinary sodium excretions following furosemide administration. The urinary sodium and dopamine excretions before and following furosemide are positively correlated in control (P < 0.05), idiopathic edema patients (P < 0.02) and in both groups combined (P < 0.005). Idiopathic edema patients have normal urinary noradrenaline and adrenaline excretions but, as previously observed, elevated: 1) plasma renin activity while either recumbent or upright, and 2) plasma aldosterone concentrations while upright. These results suggest that a decrease in urinary dopamine, a catecholamine recently recognized to have natriuretic action, possibly reflects a suppression of the renal dopaminergic system and may contribute to the excessive sodium retention in idiopathic edema either directly or indirectly through the renin-aldosterone system.

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