γ‐l‐glutamyl‐5‐hydroxy‐l‐tryptophan, but not γ‐l‐glutamyl‐l‐tryptophan, causes sodium retention in normal man

1This randomized, placebo‐controlled, cross‐over study compared the relative effectiveness of γ‐l‐glutamyl‐5‐hydroxy‐l‐tryptophan (glu‐5‐HTP) and γ‐l‐glutamyl‐l‐tryptophan (glu‐TRP) in terms of their ability to act as substrates for renal 5‐hydroxytryptamine (5‐HT) synthesis and their actions on urinary sodium excretion.

2Urinary excretion of 5‐HT and sodium were determined before, during and after 1 h intravenous infusion of an equimolar amount (45 nmol kg⁻¹ min⁻¹) of glu‐5‐HTP or glu‐TRP or placebo in nine healthy male subjects.

3Cumulative urinary 5‐HT excretion over the 4 h after the start of glu‐5‐HTP infusion was 350‐fold greater than that after placebo, and this was associated with a reduction in the urinary excretion of sodium.

4In contrast, the urinary excretion values of 5‐HT and sodium after administration of glu‐TRP were not significantly different from those observed on the placebo day.

5The marked increase in urinary 5‐HT excretion and the retention of sodium after administration of glu‐5‐HTP have been demonstrated in previous studies and result from increased intrarenal generation of 5‐HT. The absence of a rise in urinary excretion of 5‐HT after glu‐TRP infusion suggests that there was no significant conversion of this glutamyl compound to 5‐HT within the kidney. As a result, there was no effect on urinary sodium excretion.

DOI: 10.1046/j.1365-2125.1996.43412.x

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