Contributor:

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

Publisher:

Karger

Place of publishing:

Basel

Type of object:

Journal/Article

Abstract:

Adenosine (ADO) causes vasodilation in most tissues. In the kidney it can induce vasoconstriction or vasodilation, depending on the prevailing stimulation of A1 or A2 receptors (A1R, A2R). ADO-induced alterations of renal excretion may be secondary to haemodynamic changes, or reflect a direct influence on tubular transport. This whole-kidney study explored renal excretory responses to ADO receptor stimulation as related to renal haemodynamics sodium intake and cytochrome P450 (CYP-450) activity.METHODS: The effects of ADO or an A2aR agonist (DPMA) on urine flow (V), sodium excretion (UNaV) and total solute excretion were examined in anaesthetized Wistar rats on a low-sodium or high-sodium (HS) diet. Total renal blood flow (RBF; renal artery probe), and outer- and inner-medullary blood flows (OM-BF, IM-BF; laser-Doppler fluxes) were also determined.RESULTS: Consistent opposed effects of ADO and DPMA were only observed with the HS diet. ADO increased V (150%) and UNaV (100%); there were also significant increases in RBF, OM-BF and IM-BF. These changes were prevented by 1-aminobenzotriazol, a CYP-450 inhibitor. In HS rats, DPMA significantly decreased arterial blood pressure and renal excretion.CONCLUSIONS: Post-ADO diuresis/natriuresis was in part secondary to renal hyperperfusion; the response was probably mediated by CYP-450-dependent active agents. Selective A2aR stimulation induced systemic vasodilation, major hypotension, and a secondary decrease in renal excretion

Relation:

Nephron Physiology

Volume:

123

Issue:

1-2

Start page:

1

End page:

5

Detailed Resource Type:

Article

Format:

text/xml

Resource Identifier:

oai:rcin.org.pl:57120

Language:

eng

Language of abstract:

eng

Rights:

Rights Reserved - Restricted Access

Terms of use:

Copyright-protected material. Access only on terminals at the Mossakowski Medical Research Center of the Polish Academy of Sciences, may be used within the limits of statutory user freedoms.

Digitizing institution:

Mossakowski Medical Research Institute PAS

Original in:

Library of the Mossakowski Medical Research Institute PAS

Projects co-financed by:

Programme Innovative Economy, 2010-2014, Priority Axis 2. R&D infrastructure

Access:

Closed