Increased Na/H antiport activity and abundance in uremic red blood cells.
Alterations in red blood cell sodium (Na) transport have been described in chronic renal failure. This study examines the possible impact of uremia on two ouabain-insensitive pathways, the Na/H antiporter and the Cl-/NaCO3- anion exchanger. The Vmax of Na/H antiporter measured as Na influx driven by outward H gradient in acid loaded red blood cells was significantly higher in uremic red blood cells versus controls (60.5 +/- 16.5 vs. 24.5 +/- 5.4 mmol/liter cells/hr, P < 0.025). This increase in activity was associated with an increased abundance of the Na/H antiporter as determined by immunologic analysis using an affinity purified polyclonal antibody to the human NHE-1 isoform of the antiporter. By contrast, the activity of the anion exchanger measured as the DIDS-sensitive lithium (Li) influx was similar in uremic versus control red blood cells (2.10 +/- 0.18 vs. 2.14 +/- 0.20 mmol/liter cells/hr). These experiments, when considered in conjunction with prior studies showing normal Na/Li countertransport in uremia indicate that there is a selective increase in the number of functional Na/H antiporters in uremic red blood cells and that Na/Li countertransport measurements may not be a valid marker for Na/H antiporter activity in red blood cells in patients requiring dialysis for end-stage renal failure.[1]References
- Increased Na/H antiport activity and abundance in uremic red blood cells. Corry, D.B., Tuck, M.L., Nicholas, S., Weinman, E.J. Kidney Int. (1993) [Pubmed]
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