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Articles in PresS, published online ahead of print March 18, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00355.2001
Submitted on November 28, 2001
Accepted on March 11, 2002
1 Nephrological Center and Second Department of Medicine, University Medical School of Pecs, Pecs, H 7624, Hungary; Department of Physiology, West Virginia University, Morgantown, WV, USA
2 Renal Division, Emory University, Atlanta, GA, USA
3 Department of Physiology, West Virginia University, Morgantown, WV, USA
* To whom correspondence should be addressed. E-mail: cbaylis{at}wvu.edu.
We previously reported that uremic levels of urea inhibit L-arginine (L-arg) transport into endothelial cells. The present study further investigated this effect. We measured L-arg transport in cultured bovine aortic endothelial cells (BAEC) with normal or high urea (25 mM). The urea transport inhibitor phloretin abolished the inhibitory effect of urea on L-arg transport, suggesting a role for urea transporters (UTs). We screened BAEC and several other endothelial cell types for the presence of UTs by Western blot. UT-B was present in all endothelial cells, irrespective of species or location of derivation, while UT-A distribution was variable and sparse. UT-B was also abundant in rat aorta, mesenteric blood vessels and spinotrapezius muscle, while UT-A distribution was, again, variable and sparse. Chronic elevation of urea had variable, inconsistent effects on UT abundance. This study showed that urea must enter endothelial cells, probably by UT-B, in order to inhibit L-arg transport. In view of the wide distribution of UT-B in rat vasculature, elevated BUN may lead to endothelial L-arg deficiency in vivo.
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