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1 Department of Pharmacy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto 606 - 8507; and 2 Department of Laboratory Medicine, School of Medicine, University of Tokushima, Tokushima 770 - 8503, Japan
First published August 21, 2001;
10.1152/ajprenal.0346.2001.
The progression of renal damage resulting
from reduced nephron mass has been extensively studied in the 5/6
nephrectomized rat. However, reabsorption of small peptides and
D-glucose across the renal proximal tubule in this model
remains poorly understood. In this study, we examined the alterations
of H+-peptide cotransporters (PEPT1 and PEPT2) and
Na+-D-glucose cotransporters (SGLT1 and SGLT2)
in chronic renal failure. Two weeks after surgery,
H+-dependent [14C]glycylsarcosine uptake by
the renal brush-border membrane vesicles isolated from 5/6
nephrectomized rats was significantly increased compared with that from
sham-operated controls. Kinetic analysis revealed that the maximum
velocity value for [14C]glycylsarcosine uptake by the
high-affinity-type of peptide transporter was increased threefold by
5/6 nephrectomy, without significant changes in the apparent
Michaelis-Menten constant value. Competitive PCR analyses indicated
that the expression of PEPT2 mRNA was markedly increased in the remnant
kidney, but PEPT1, SGLT1, and SGLT2 mRNA levels showed no
significant changes. These findings indicated that the
high-affinity-type H+-peptide cotransport activity is
upregulated by 5/6 nephrectomy, accompanied by the increased expression
of PEPT2. The upregulation of PEPT2 expression would result in an
increase in reabsorption of small peptides and peptide-like drugs
across the brush-border membranes in chronic renal failure.
5/6 nephrectomy; renal ablation; renal failure; renal tubular reabsorption; peptide-like drug; high-affinity H+-peptide cotransporter
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