Tclk. Wa et al., GAMMA-L-GLUTAMYL-5-HYDROXY-L-TRYPTOPHAN, BUT NOT GAMMA-L-GLUTAMYL-L-TRYPTOPHAN, CAUSES SODIUM RETENTION IN NORMAL MAN, British journal of clinical pharmacology, 42(3), 1996, pp. 365-370
1 This randomized, placebo-controlled, cross-over study compared the r
elative effectiveness of gamma-L-glutamyl-5-hydroxy-L-tryptophan (glu-
5-HTP) and gamma-L-glutamyl-L-tryptophan (glu-TRP) in terms of their a
bility to act as substrates for renal 5-hydroxytryptamine (5-HT) synth
esis and their actions on urinary sodium excretion. 2 Urinary excretio
n of 5-HT and sodium were determined before, during and after 1 h intr
avenous infusion of an equimolar amount (45 nmol kg(-1) min(-1)) of gl
u-5-HTP or glu-TRP or placebo in nine healthy male subjects. 3 Cumulat
ive urinary 5-HT excretion over the 4 h after the start of glu-5-HTP i
nfusion was 350-fold greater than that after placebo, and this was ass
ociated with a reduction in the urinary excretion of sodium. 4 In cont
rast, the urinary excretion values of 5-HT and sodium after administra
tion of glu-TRP were not significantly different from those observed o
n the placebo day. 5 The marked increase in urinary 5-HT excretion and
the retention of sodium after administration of glu-5-HTP have been d
emonstrated in previous studies and result from increased intrarenal g
eneration of 5-HT. The absence of a rise in urinary excretion of 5-HT
after glu-TRP infusion suggests that there was no significant conversi
on of this glutamyl compound to 5-HT within the kidney. As a result, t
here was no effect on urinary sodium excretion.