The recovery of renal function in renal transplant recipients is accompanie
d by an enhanced ability to synthesize dopamine (DA), which may contribute
to maintain sodium homeostasis. Patients suffering from chronic renal paren
chymal disease, a well-recognized form of salt sensitive (SS) hypertension,
have a reduced ability to produce DA that correlates well with deteriorati
on of renal function. In patients afflicted with IgA nephropathy, but norma
l renal function, urinary excretion of DA correlated positively with BP res
ponses to changes from 200 to 20 mmol/day salt intake. In black salt resist
ant (SR) normotensives (NT) and SR hypertensives, under low salt intake (40
mmol/day), but not SS-NT and SS-HT, the saline infusion induced increments
of DA and DOPAC urinary excretion correlated significantly with increments
of sodium urinary excretion and sodium fractional excretion. Patients affl
icted with heart failure (HF) have a reduced delivery of L-DOPA to the kidn
ey, accompanied by an increase in DA/L-DOPA urinary ratios. This suggests t
hat HF patients have an increased ability to take up or decarboxylate L-DOP
A. Sodium restriction resulted in a significant decrease in urinary L-DOPA,
DA and DOPAC in HF patients, suggesting that the system responds to sodium
. It is concluded that activity of renal dopaminergic system may be altered
in SS subjects, despite the level of their BP, and an enhanced delivery of
L-DOPA to the kidney may be beneficial in edema formation states.