HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Accepted manuscript (PDF) All Versions of this Article: JOE-08-0260v1 198/3/617    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Abdel-Razik, A. Articles by Ashton, N. Search for Related Content PubMed PubMed Citation Articles by Abdel-Razik, A. Articles by Ashton, N.

A Abdel-Razik, Manchester, United States
E Forty, Faculty of Life Sciences, University of Manchester, Manchester, United Kingdom
R Balment, Faculty of Life Sciences, University of Manchester, Manchester, United Kingdom
N Ashton, University of Manchester, Faculty of Life Sciences, Manchester, United Kingdom

Correspondence: Nick Ashton, Email: nick.ashton{at}manchester.ac.uk

Abstract

Urotensin II (UII) is a potent vasoactive peptide that was originally identified in teleost fish. Mammalian orthologs of UII and its receptor (UT) have been described in several species, including humans and rats. We have shown previously that bolus injections of UII caused a decrease in urine flow and sodium excretion rates in parallel with marked reductions in renal blood flow (RBF) and glomerular filtration rate (GFR). The aim of this study was to determine the effect of UII infusion at a dose that has minimal impact upon renal haemodynamics in order to identify a potential direct tubular action of UII. Infusion of rat UII (rUII) at 0.6 pmol.min-1.100g body weight-1 in male Sprague Dawley rats, which had no effect on RBF and caused a 30% reduction in GFR, resulted in a significant increase in the fractional excretion of sodium (vehicle 2.3 ± 0.6 vs rUII 0.6 pmol 4.5 ± 0.6 %, P<0.05) and potassium. At the higher dose of 6 pmol.min-1.100g body weight-1, haemodynamic effects dominated the response. rUII induced a marked reduction in RBF and GFR (vehicle 1.03 ± 0.06 vs rUII 6 pmol 0.31 ± 0.05 ml.min-1.100g body weight-1, P<0.05) resulting in an antidiuresis and antinatriuresis, but no change in fractional excretion of sodium or potassium. UII and UT mRNA expression were greater in the renal medulla compared with the cortex. Together, these data support an inhibitory action of UII on renal tubule sodium and potassium reabsorption in the rat, in addition to its previously described renal haemodynamic effects.

This article has been cited by other articles:

				A. E. S. Abdel-Razik, R. J. Balment, and N. Ashton Enhanced renal sensitivity of the spontaneously hypertensive rat to urotensin II Am J Physiol Renal Physiol, October 1, 2008; 295(4): F1239 - F1247. [Abstract] [Full Text] [PDF]