Heart failure, aging, and renal synthesis of dopamine

Am J Kidney Dis. 2001 Sep;38(3):502-9. doi: 10.1053/ajkd.2001.26834.

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.

MeSH terms

  • 3,4-Dihydroxyphenylacetic Acid / blood
  • 3,4-Dihydroxyphenylacetic Acid / urine
  • Adult
  • Age Factors
  • Aged
  • Aging / blood
  • Aging / physiology
  • Aging / urine*
  • Aldosterone / blood
  • Aldosterone / urine
  • Cardiac Output, Low / blood
  • Cardiac Output, Low / physiopathology
  • Cardiac Output, Low / urine*
  • Case-Control Studies
  • Creatinine / urine
  • Diet, Sodium-Restricted
  • Dopamine / biosynthesis
  • Dopamine / blood
  • Dopamine / urine*
  • Echocardiography
  • Female
  • Homovanillic Acid / blood
  • Homovanillic Acid / urine
  • Humans
  • Kidney / metabolism*
  • Kidney / physiopathology
  • Levodopa / blood
  • Levodopa / urine
  • Male
  • Middle Aged
  • Norepinephrine / blood
  • Norepinephrine / urine
  • Statistics as Topic
  • Urine

Substances

  • 3,4-Dihydroxyphenylacetic Acid
  • Levodopa
  • Aldosterone
  • Creatinine
  • Dopamine
  • Norepinephrine
  • Homovanillic Acid