title: Adenosine effects on renal function in the rat: role of sodium intake and cytochrome P450.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
authors.forename: Marta
authors.initials: M
authors.lastname: Kuczeriszka
authors.forename: Leszek
authors.initials: L
authors.lastname: Dobrowolski
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Walkowska
authors.forename: Janusz
authors.initials: J
authors.lastname: Sadowski
authors.forename: Elżbieta
authors.initials: E
authors.lastname: Kompanowska-Jezierska
mesh_terms: D000241:Adenosine / Q000031:analogs & derivatives / Q000494:pharmacology*; D058908:Adenosine A2 Receptor Agonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism*; D004231:Diuresis / Q000187:drug effects; D007668:Kidney / Q000187:drug effects* / Q000502:physiology*; D008297:Male; D009318:Natriuresis / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D018047:Receptors, Purinergic P1 / Q000378:metabolism; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology; D012964:Sodium / Q000652:urine*; D012982:Sodium, Dietary / Q000008:administration & dosage
chemical_list: D058908:Adenosine A2 Receptor Agonists; D018047:Receptors, Purinergic P1; D012982:Sodium, Dietary; C056426:CGS 24012; D003577:Cytochrome P-450 Enzyme System; D012964:Sodium; D000241:Adenosine