Heart failure, aging, and renal synthesis of dopamine

Abstract

The present study evaluates renal dopaminergic activity in 23 patients with heart failure (HF), 10 age-matched controls, and 10 young subjects during normal-salt (NS) intake and after 8 days of low-salt (LS) intake (patients with HF and age-matched controls only). LS intake produced a marked reduction in urine volume in patients with HF but failed to affect urine volume in age-matched controls. Urinary sodium and fractional excretion of sodium were markedly reduced by LS intake in patients with HF and age-matched controls. Daily urinary excretion of l-3,4-dihydroxyphenylalanine (l-dopa) and dopamine was lower in patients with HF than in age-matched controls. LS intake failed to alter l-dopa and dopamine urinary excretion in control subjects. In patients with HF, LS intake produced a significant decrease in urinary l-dopa excretion, but failed to alter the urinary excretion of dopamine. No significant differences were observed in urinary l-dopa, dopamine, and dopamine metabolite levels between aged controls and young healthy subjects. Urinary dopamine-l-dopa ratios in patients with HF on LS intake (24.5 ± 7.1) were significantly greater than those with NS intake (11.6 ± 1.3). Urinary dopamine-l-dopa ratios in old control subjects (LS, 9.7 ± 1.3; NS, 9.3 ± 1.1) did not differ from those in young healthy subjects (9.2 ± 0.8). LS intake produced a marked increase in plasma aldosterone levels in both patients with HF (84.6 ± 14.4 to 148.2 ± 20.4 pg/mL; P = 0.0008) and controls (102.1 ± 13.4 to 151.6 ± 15.7 pg/mL; P < 0.04). Plasma norepinephrine levels were not significantly affected by LS intake in controls (5.1 ± 1.62 to 6.3 ± 1.6 pmol/mL; P = 0.22), but were significantly increased in patients with HF (5.8 ± 0.8 to 7.1 ± 0.9 pmol/mL; P = 0.04). In conclusion, patients with HF are endowed with an enhanced ability to take up (or decarboxylate) filtered l-dopa, which might counterbalance the reduced renal delivery of l-dopa, contributing to a relative preservation of dopamine synthesis. This may result as a compensatory mechanism, activated by stimuli leading to sodium reabsorption. Age seems to have no influence on renal dopamine production. © 2001 by the National Kidney Foundation, Inc.