Skip Navigation


NDT Advance Access originally published online on June 7, 2007
Nephrology Dialysis Transplantation 2007 22(10):2805-2809; doi:10.1093/ndt/gfm322
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
22/10/2805    most recent
gfm322v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Dobrowolski, L.
Right arrow Articles by Sadowski, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dobrowolski, L.
Right arrow Articles by Sadowski, J.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org



Sodium intake determines the role of adenosine A2 receptors in control of renal medullary perfusion in the rat

Leszek Dobrowolski, Elzbieta Kompanowska-Jezierska, Agnieszka Walkowska and Janusz Sadowski

Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

Correspondence and offprint requests to: Leszek Dobrowolski, Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Pawinskiego 5, 02-106 Warsaw, Poland. Email: lesdobro{at}cmdik.pan.pl



  Abstract

Background. In the kidney, adenosine (ADO) can induce either vasoconstriction or vasodilatation, mediated by A1 or A2 receptors, respectively. The vasodilator influence may be of special importance in the renal medulla which operates at low tissue pO2 levels and is susceptible to ischaemic damage. It has not been established if ADO induced vasodilatation is modified by salt intake.

Methods. We examined effects of stimulation or inhibition of ADO receptors (A2R) on perfusion of the renal cortex and medulla on low- or high- sodium intake (LS, HS). Effects of suprarenal aortic ADO (0.03 mmol/kg/h), A2R agonist (DPMA), 0.08–0.4 mmol/kg/h, or antagonist (DMPX), 1.7 µmol/kg/h, were examined in anaesthetized rats maintained on LS (0.15% Na) or HS (4% Na) diet for 3 weeks. Whole kidney blood flow (RBF) and the perfusion (laser-Doppler) of the superficial cortex and outer and inner medulla (OM-BF, IM-BF) were measured.

Results. In LS rats neither drug changed renal perfusion. In HS rats ADO increased RBF 18 ± 3%, OM-BF 16 ± 7% and IM-BF 16 ± 6%. IM-BF increased after DPMA 18 ± 5% and decreased after DMPX 13 ± 3%; neither drug consistently changed perfusion of the cortex.

Conclusions. On HS intake, medullary perfusion is controlled by ADO vasodilator (A2) receptors, which may help provide adequate oxygen to the medulla, the zone which normally operates under relative hypoxia. On LS intake, the vasodilator and vasoconstrictor effects are probably in balance and ADO has little role in control of intrarenal circulation.

Keywords: adenosine; adenosine A2 receptors; laser-Doppler measurement; renal blood flow; renal medullary blood flow; salt intake

Received for publication: 22. 3.07
Accepted in revised form: 2. 5.07


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.