Renal synthesis of dopamine in asymptomatic post-infarction left ventricular systolic dysfunction

Left ventricular systolic dysfunction (LVSD) following acute myocardial infarction (AMI), by decreasing renal blood flow, may interfere with renal (L)-DOPA availability and, consequently, dopamine synthesis. Dopamine of renal origin exerts local natriuretic effects. We studied 17 post-AMI patients with asymptomatic LVSD (ejection fraction < 40%) and 14 without (ejection fraction greater than or equal to 40%), measuring 24-h urinary excretions of (L)-DOPA, dopamine and its metabolites, and plasma levels of the amines, amine derivatives and type-B natriuretic peptide (BNP). Baseline characteristics were well balanced between the two groups. No differences were observed in urinary volume and sodium and creatinine excretions. The group with asymptomatic LVSD presented lower urinary excretion of (L)-DOPA (66.8 +/- 10.1 versus 115.3 +/- 21.9 nmol,day(-1), P = 0.04), whereas plasma levels of (L)-DOPA were identical in both groups. Urinary dopamine was similar in the two groups (1124.2 +/- 172.4 versus, 1049.0 +/- 146.4 nmol.day(-1), P = 0.86), resulting in higher urinary dopamine/(L)-DOPA ratios in patients with asymptomatic LVSD (20.4 +/- 3.0 versus 9.9 +/- 0.8, P < 0.001). Plasma levels of BNP were higher in the asymptomatic LVSD group (348.5 +/- 47.3 versus 146.8 +/- 21.9 pg.ml(-1), P = 0.003). Ejection fraction was negatively correlated with both plasma levels of BNP and urinary dopamine/L-DOPA ratios. Renal dopamine production is well preserved in patients with asymptomatic LVSD and increased neurohumoral activation, despite reduced urinary excretion of its precursor. This suggests that renal uptake and/or decarboxylation of (L)-DOPA is enhanced in this condition, as a compensatory mechanism, contributing to preservation of urinary sodium excretion.