Arginine transport is augmented, through modulation of cationic amino acid transporter-1, in obstructive uropathy in rats

Idit F. Schwartz, Aharon Davidovitz, Tamara Chernichovski, Nomi Levin-Iaina, Hanan Guzner-Gur, Yoram Levo, Doron Schwartz

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

Background: The decrease in glomerular filtration rate (GFR), which is characteristic of obstructive uropathy, was suggested to be associated with attenuated nitric oxide (NO) generation. Since availability of L-arginine, the sole precursor for NO, governs NO synthesis, we aimed to determine the role of glomerular arginine transport in rats subjected to 24 h of bilateral ureteral ligation (BUO). Methods: Glomerular arginine transport was measured by uptake of radiolabeled arginine ([3H]-L-arginine), cationic amino acid transporters (CAT)-1 and -2 and arginases I and II mRNA expression were determined using reverse transcription-polymerase chain reaction. CAT-1, arginase I, and arginase II protein contents were evaluated by Western blotting. Results:L-Arginine transport by freshly harvested glomeruli from BUO rats was significantly augmented than in controls. The aforementioned findings were associated with a significant increase in glomerular CAT-1 mRNA expression, while CAT-2 mRNA was unchanged. Western blotting demonstrated a significant increase in CAT-1 abundance in BUO. Expression of both glomerular arginase I and II mRNA and protein content were significantly elevated in BUO. Conclusions: BUO induces an increase in glomerular arginine transport via upregulation of CAT-1, probably due to increase in arginine utilization by a non-NO pathway.

Original languageEnglish
Pages (from-to)210-216
Number of pages7
JournalKidney and Blood Pressure Research
Volume31
Issue number3
DOIs
StatePublished - Jul 2008

Keywords

  • Acute renal failure
  • Nitric oxide
  • Renal hemodynamics

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