title: 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.
authors.affiliation: Unidade de Investigação e Desenvolvimento Cardiovascular do Porto, Portugal. pbettfer@esoterica.pt
authors.forename: A
authors.initials: A
authors.lastname: Ferreira
authors.forename: P
authors.initials: P
authors.lastname: Bettencourt
authors.forename: M
authors.initials: M
authors.lastname: Pestana
authors.forename: F
authors.initials: F
authors.lastname: Correia
authors.forename: P
authors.initials: P
authors.lastname: Serrão
authors.forename: L
authors.initials: L
authors.lastname: Martins
authors.forename: M
authors.initials: M
authors.lastname: Cerqueira-Gomes
authors.forename: P
authors.initials: P
authors.lastname: Soares-Da-Silva
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000097:blood / Q000652:urine; D000328:Adult; D000367:Age Factors; D000368:Aged; D000375:Aging / Q000097:blood / Q000502:physiology / Q000652:urine*; D000450:Aldosterone / Q000097:blood / Q000652:urine; D002303:Cardiac Output, Low / Q000097:blood / Q000503:physiopathology / Q000652:urine*; D016022:Case-Control Studies; D003404:Creatinine / Q000652:urine; D004039:Diet, Sodium-Restricted; D004298:Dopamine / Q000096:biosynthesis / Q000097:blood / Q000652:urine*; D004452:Echocardiography; D005260:Female; D006719:Homovanillic Acid / Q000097:blood / Q000652:urine; D006801:Humans; D007668:Kidney / Q000378:metabolism* / Q000503:physiopathology; D007980:Levodopa / Q000097:blood / Q000652:urine; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood / Q000652:urine; D013223:Statistics as Topic; D014556:Urine
chemical_list: D015102:3,4-Dihydroxyphenylacetic Acid; D007980:Levodopa; D000450:Aldosterone; D003404:Creatinine; D004298:Dopamine; D009638:Norepinephrine; D006719:Homovanillic Acid