Demethylation of 3-O-methyldopa in the kidney: A possible source for dopamine in urine

Document Type

Journal Article

Publication Date

1-1-1996

Journal

American Journal of Physiology

Volume

270

Issue

5 PART 2

DOI

10.1152/ajprenal.1996.270.5.f862

Abstract

The possibility that demethylation of 3-O-methyldopa (OM-dopa) in the kidney could provide a source for dopamine in the urine was explored in male Wistar rats aged 60-90 days, using in vivo and in vitro approaches. The results showed that endogenous OM-dopa is filtered, reabsorbed and extensively metabolized in the kidney. Infusion of OM-dopa into anesthetized rats increased significantly urinary excretion of Na+, dopa, dopamine, and 3,4 dihydroxyphenylacetic acid. Whole kidney homogenates, slices from renal cortex, and microdissected proximal tubules produced significant amounts of both dopa and dopamine when incubated with OM-dopa. Renal cortex slices produced dose-dependent amounts of dopa and dopamine when incubated with 1-100 μM OM-dopa. Incubation of microdissected proximal tubule segments with 1 μM OM-dopa produced a fourfold (P < 0.025) increment in dopa and a twofold (P < 0.05) increment in dopamine (an effect similar to that observed with 1 μM L-dopa). One micromolar OM-dopa or 1 μM L-dopa decreased (P < 0.05) Na+-K+-adenosinetriphosphatase activity measured at maximal velocity condition in proximal tubules. In conclusion, these experiments show that in vitro the kidney is able to produce dopamine by demethylation of OM-dopa, while the results of the OM-dopa infusion suggest that this conversion may also occur in vivo. sodium; dopa; proximal tubules; sodium-potassium ionadenosinetriphosphatase activity; renal cortex slices; infusion Copyright © 1996 the American Physiological Society.

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