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Articles in PresS, published online ahead of print October 15, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00174.2002
Submitted on May 2, 2002
Accepted on October 9, 2002
1 Department of Marine Biomedicine and Environmental Science, Medical University of South Carolina, Charleston, SC, USA
2 Department of Medicine, Medical University of South Carolina, Charleston, SC, USA
3 Department of Pharmacology and Experimental Therapeutics, Medical University of South Carolina, Charleston, SC, USA
4 Department of Medicine, Medical University of South Carolina, Charleston, SC, USA; Ralph H. Johnson Veteran's Affairs Medical Center, Charleston, SC, USA
* To whom correspondence should be addressed. E-mail: fitzgiwr{at}musc.edu.
In general, marine elasmobranch fishes (sharks, skates and rays) maintain body fluid osmolality above seawater principally by retaining large amounts of urea. Maintenance of the high urea concentration is due in large part to efficient renal urea reabsorption. Regulation of renal urea reabsorption also appears to play a role in the maintenance of fluid homeostasis of elasmobranchs that move between habitats of different salinities. We identified and cloned a novel, 2.7-kb cDNA from the kidney of the euryhaline, Atlantic stingray, Dasyatis sabina(Genbank accession no, AF443781). This cDNA putatively encoded a 431 amino acid protein (strUT-1) that had a high degree of sequence identity (71%) to the shark kidney facilitated urea transporter. However, the predicted carboxy-terminal region of strUT-1 appears to contain an additional sequence that is unique among cloned renal urea transporters. Injection of strUT-1 cRNA into Xenopus oocytes induced a 33-fold increase in [ 14 C]-urea uptake that was inhibited by phloretin. Four mRNA bands were detected in kidney by Northern blot; a predominant transcript at 2.7 kb corresponding to the expected size of strUT-1 mRNA and minor bands at 2.2, 3.5 and 5.0 kb. The identification of a facilitated urea transporter in the kidney of the Atlantic stingray provides further support for the proposal that passive mechanisms contribute to urea reabsorption by the elasmobranch kidney.
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