HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Free Full Text (PDF) Free 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 Walkowska, A. Articles by Sadowski, J. Search for Related Content PubMed PubMed Citation Articles by Walkowska, A. Articles by Sadowski, J.

---

ORIGINAL RESEARCH ARTICLE

A BRIEF COMMUNICATION

Role of NO and COX Pathways in Mediation of Adenosine A1 Receptor–Induced Renal Vasoconstriction

Agnieszka Walkowska¹, Leszek Dobrowolski, Elbieta Kompanowska-Jezierska and Janusz Sadowski

Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, 02-106 Warsaw, Poland

To whom requests for reprints should be addressed at ¹ Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Pawiskiego 5, 02-106 Warsaw, Poland. E-mail: renal{at}cmdik.pan.pl

The mechanism of adenosine A1 receptor–induced intrarenal vasoconstriction is unclear; it depends on sodium intake and may be mediated by changing the intrarenal activity of the nitric oxide (NO) and/or cyclooxygenase (COX) pathway of arachidonic acid metabolism. The effects of 2-chloro-N⁶-cyclopentyl-adenosine (CCPA), a selective A1 receptor agonist, on renal hemodynamics were examined in anesthetized rats maintained on high sodium (HS) or low sodium (LS) diet. Total renal (i.e., cortical) blood flow (RBF) as well as superficial cortical (CBF), outer medullary (OMBF), and inner medullary (IMBF) flows were determined by laser-Doppler. In HS rats, suprarenal aortic infusions of 8–40 nmol/kg/hr CCPA decreased IMBF (15%) and other perfusion indices (22%–27%); in LS rats, IMBF increased 3% (insignificant) and other indices decreased 13%–24%. In LS rats, pretreatment with N-nitro-L-arginine methyl ester prevented the A1 receptor–mediated decrease in RBF and CBF but not OMBF; the response in IMBF was not altered. Pretreatment with indomethacin prevented the decreases in RBF, CBF, and OMBF and did not change the response of IMBF. Thus, within the cortex the vasoconstriction that follows A1 receptor activation results both from inhibition of NO synthesis and from stimulation of vasoconstrictor products of the COX pathway. In the outer medulla, the latter products seem exclusively responsible for CCPA-induced vasoconstriction. The observation that in LS rats IMBF was not affected by stimulation of adenosine A1 receptors suggests that limiting salt intake may help protect medullary perfusion against vasoconstrictor stimuli which have the potential to disturb long-term control of arterial pressure.

Key Words: renal cortical blood flow • renal medullary blood flow • adenosine A1 receptor agonist • nitric oxide • COX

This article has been cited by other articles:

				A. Kulick, C. Panico, P. Gill, and W. J. Welch Low salt intake increases adenosine type 1 receptor expression and function in the rat proximal tubule Am J Physiol Renal Physiol, July 1, 2008; 295(1): F37 - F41. [Abstract] [Full Text] [PDF]

				L. Dobrowolski, E. Kompanowska-Jezierska, A. Walkowska, and J. Sadowski Sodium intake determines the role of adenosine A2 receptors in control of renal medullary perfusion in the rat Nephrol. Dial. Transplant., October 1, 2007; 22(10): 2805 - 2809. [Abstract] [Full Text] [PDF]