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

Abstract

1 The effect of oral lithium (300 mg) on the renal response to the selective DA1-dopamine receptor agonist fenoldopam was investigated in seven normal men. Lithium had no influence on sodium excretion and renal haemodynamics during fenoldopam infusion. The fenoldopam-induced rise in PRA was enhanced in the presence of lithium. We conclude that a previously described interaction between lithium and the dopamine agonist gludopa is not mediated by DA l-dopamine receptors or is confined to higher doses of lithium.

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

“…Lithium and the renal response to gludopa, fenoldopam and dopamine Schoors & Dupont (1990) provide very interesting data on the lack of effect of lithium on the renal response to dopamine, which were not published before we wrote our report (Girbes et al, 1990). These data support our speculation that the interaction between lithium and the dopamine prodrug gludopa is not mediated by (proximal tubular) dopamine DA1-receptors.…”

“…Therefore, in the in vivo situation, the increase in PRA after fenoldopam could, at least in part, be related to the fall in blood pressure, resulting in a baroreflex-mediated increase in sympathetic tone, and hence Padrenoceptor-mediated renin release. Girbes et al (1990) did not provide any data on the blood pressure response to fenoldopam, but others have observed marked reductions in blood pressure in healthy volunteers, using similar doses (Allison et al, 1987). Using an infusion rate of fenoldopam of 0.05 ,ug kg-' min-1, a nondepressor dose which increases renal blood flow, Hughes et al (1988) could not demonstrate any change in PRA.…”

“…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.These explanations both seem very unlikely in view of our results concerning the effect of lithium on the renal response to dopamine (Schoors & Dupont, 1990). Using a similar design and the same dose of lithium carbonate as Jeffrey, resulting in similar lithium levels, we did not find any effect of lithium pretreatment on the natriuretic response to dopamine infusion.…”

“…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.…”

“…

651Lithium and the natriuretic response to gludopa, fenoldopam and dopamine Girbes et al (1990) recently reported that oral lithium (300 mg) had no effect on the renal response to DA1-dopamine receptor stimulation, by fenoldopam, in normal man. 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.

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