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

Left ventricular systolic dysfunction (LVSD) following acute myocardial inf arction (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 w ith asymptomatic LVSD (ejection fraction < 40%) and 14 without (ejection fr action greater than or equal to 40%), measuring 24-h urinary excretions of (L)-DOPA, dopamine and its metabolites, and plasma levels of the amines, am ine derivatives arid type-B natriuretic peptide (BNP). Baseline characteris tics were well balanced between the two groups. No differences were observe d in urinary volume and sodium and creatinine excretions. The group with as ymptomatic 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 = 0.8 6), resulting in higher urinary dopamine/(L)-DOPA ratios in patients with a symptomatic LVSD (20.4 +/- 3.0 versus 9.9 +/- 0.8, P < 0.001). Plasma level s 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 corr elated with both plasma levels of BNP and urinary dopamine/L-DOPA ratios. R enal dopamine production is well preserved in patients with asymptomatic LV SD and increased neurohumoral activation, despite reduced urinary excretion of its precursor. This suggests that renal uptake and/or decarboxylation o f (L)-DOPA is enhanced in this condition, as a compensatory mechanism, cont ributing to preservation of urinary sodium excretion.