The effect of lithium on the renal response to the dopamine prodrug gludopa in normal man.

Abstract

1. The effect of oral lithium on the renal response to gamma‐L‐glutamyl‐ L‐dopa (gludopa, 25 micrograms kg‐1 min‐1) was investigated in seven normal males. 2. Gludopa at this dose produced an 800‐fold increase in urine dopamine excretion. It was natriuretic and suppressed plasma renin activity without altering blood pressure and pulse. 3. Lithium alone increased sodium excretion and stimulated plasma renin activity. However, it abolished the natriuresis produced by gludopa. 4. Gludopa did not significantly affect lithium clearance. 5. This study suggests that lithium interacts with dopamine at the proximal tubule and that the lithium clearance method is not suitable for investigating dopaminergic mechanisms in the kidney.

Lithium and the natriuretic response to gludopa, fenoldopam and dopamine [letter; comment]

“…These results contrast with an earlier report by Jeffrey et al (1988) that lithium (in a higher dose of 750 mg) abolished the natriuretic response to the renal dopamine prodrug gludopa, suggesting that lithium interacts with dopamine at the proximal tubule. Girbes et al (1990) concluded that the interaction between lithium and the dopamine prodrug gludopa is not mediated by DA1-dopamine receptors or is confined to higher doses of lithium.…”

“…Furthermore, some caution with the interpretation of the results of Schoors & Dupont (1990) is required, because they did not find any natriuretic effect of lithium alone. This is in contrast with our results and those of Jeffrey et al (1988). Possibly there is a difference in salt status of the subjects studied at the beginning of the studies, which might influence the results.…”

“…In fact Schoors & Dupont (1990) observe a higher sodium excretion at baseline during the study day without lithium than was observed in our (Girbes et al, 1990) and Jeffrey et al's (1988) study. Schoors & Dupont (1990) as well as Jeffrey et al (1988) found higher levels of PRA in the group with lithium pretreatment, which might play a role in the abolished natriuretic response to gludopa, through increased aldosterone secretion. Some evidence, however, suggests that lithium induces a relative resistance to the action of aldosterone on the distal nephron (Singer, 1981).…”

Lack of effect of lithium on the renal response to DA1‐dopamine receptor stimulation by fenoldopam in normal man [see comments]

“…However, no significant changes occurred in this study with seven volunteers. In the study of Jeffrey et al (1988) Cavero et al (1987) demonstrated a rise of PRA by direct DA1 stimulation. The extent of increase in PRA during fenoldopam infusion was influenced by the presence of lithium and suggests that lithium enhances the effects of DA1-dopamine stimulation.…”

“…A recent publication (Jeffrey et al, 1988) suggests that lithium interacts with dopamine at the proximal tubule.…”