Nephrology Dialysis Transplantation, Vol 12, Issue 9 1921-1927, Copyright © 1997 by Oxford University Press
S Riley, N Talbot, M Ahmed, K Jouhl and B Hendry
Background. Membrane transport of choline cations is
elevated in renal failure in erythrocytes and cerebral tissue but the
origins and clinical importance of this are unknown.
Methods. The membrane transport changes have been
characterized using erythrocytes from patients on maintenance haemodialysis
(HD), patients on continuous ambulatory peritoneal dialysis (CAPD), and
control subjects. Data were obtained from cells depleted of intracellular
choline to create zero-trans (ZT) conditions for
choline influx. [14C]-choline influx measurements
provided a kinetic description of choline flux as the sum of a saturable
transport system (defined by Vmax and Km) and an apparent diffusion
pathway. Inhibition of choline transport by hemicholinium-3 (HC-3), quinine
and N-ethylmaleimide (NEM) has been studied. Actions of three cationic
polyamine putative uraemic toxins (putrescine, spermidine, spermine) were
tested in control erythrocytes. Results. Mean (SEM)
Vmax (ZT) was increased in HD at 45.0 (3.0) &mgr;mol/l cells/h and in
CAPD at 46.6 (2.5) &mgr;mol/l cells/h compared to controls (30.0 (2.0)
&mgr;mol/l cells/h). Mean Km (ZT) was not significantly altered in HD
or CAPD (HD: 6.1 (1.6) &mgr;M; CAPD: 5.5 (0.7) &mgr;M; control: 5.1
(0.9) &mgr;M). The sensitivity of choline transport to the inhibitors
tested was not altered in HD. 1.0 mM quinine, 2.0 mM NEM and 1.0 mM HC-3
caused 75-90% inhibition of transport in both HD and controls. For
inhibition of ZT influx of 25 &mgr;M choline the mean IC50 of quinine
was 90 (9) &mgr;M in HD and 101 (13) &mgr;M in controls (n.s.). the
ZT influx of 200 &mgr;M choline was not altered by any of the
polyamines at concentrations up to 1.0 mM.
Conclusions. Membrane choline transport in CRF remains
protein-mediated and exhibits normal substrate and inhibitor affinities;
high values of Vmax seem to occur through increased surface expression of
an active normal choline transporter. Increases in plasma polyamines cannot
explain the choline transport changes in CRF.
Keywords: choline; chronic renal failure; erythrocyte;
membrane transport; polyamines; uraemia
ORIGINAL ARTICLES
Characterization of human erythrocyte choline transport in chronic renal failure
Renal Group, Department of Medicine, King's College School of Medicine and Dentistry, Bessemer Road, London SE5 9PJ, UK; Corresponding author
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