title: Effects of ATP on rat renal haemodynamics and excretion: role of sodium intake, nitric oxide and cytochrome P450.
abstract: OBJECTIVE
  Adenosine-5'-triphosphate (ATP) affects intrarenal vascular tone and tubular transport via P2 receptors; however, the actual role of the system in regulation of renal perfusion and excretion remains unclear and is the subject of this whole-kidney study.
  
  
  METHODS
  Effects of suprarenal aortic ATP infusion, 0.6-1.2 mg kg(-1) h(-1), were examined in anaesthetised rats maintained on low- (LS) or high-sodium (HS) diet. Renal artery blood flow (RBF, transonic flow probe) and the perfusion (laser-Doppler flux) of the superficial cortex (CBF) and outer and inner medulla (OM-BF, IM-BF) were measured, together with sodium and water excretion and urine osmolality.
  
  
  RESULTS
  Adenosine-5'-triphosphate did not change arterial pressure, RBF or CBF while the effects on medullary perfusion depended on sodium intake. In LS rats ATP increased IM-BF 19 +/- 6%, the effect was prevented by inhibition of nitric oxide (NO) with N-nitro-l-arginine methyl ester. In HS rats ATP decreased OM-BF 16 +/- 3% and IM-BF (7 +/- 4%, not significant); previous inhibition of cytochrome P450 with 1-aminobenzotriazol blunted the OM-BF decrease and reversed the previous decrease of IM-BF to a 13 +/- 8% increase. Inhibition of P2 receptors with pyridoxal derivative (PPADS) abolished medullary vascular responses to ATP. In HS rats pre-treated with PPADS, ATP increased tubular reabsorption, probably via adenosine formation and stimulation of P1 receptors.
  
  
  CONCLUSIONS
  The data indicate a potential role of ATP in the selective control of renal medullary perfusion, different in sodium depleted and sodium replete rats. The action of ATP appears to be mediated by the NO system and the cytochrome P450 dependent vasoactive metabolites.
authors.affiliation: Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland. lesdobro@cmdik.pan.pl
authors.forename: L
authors.initials: L
authors.lastname: Dobrowolski
authors.forename: A
authors.initials: A
authors.lastname: Walkowska
authors.forename: E
authors.initials: E
authors.lastname: Kompanowska-Jezierska
authors.forename: M
authors.initials: M
authors.lastname: Kuczeriszka
authors.forename: J
authors.initials: J
authors.lastname: Sadowski
mesh_terms: D000255:Adenosine Triphosphate / Q000008:administration & dosage*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D065607:Cytochrome P-450 Enzyme Inhibitors; D003577:Cytochrome P-450 Enzyme System / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects / Q000502:physiology*; D007672:Kidney Cortex / Q000187:drug effects / Q000502:physiology; D007679:Kidney Medulla / Q000187:drug effects / Q000502:physiology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D009994:Osmolar Concentration; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D058919:Purinergic P2 Receptor Antagonists; D011732:Pyridoxal Phosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology; D012964:Sodium / Q000652:urine; D012982:Sodium, Dietary / Q000008:administration & dosage*; D014230:Triazoles / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology
chemical_list: D065607:Cytochrome P-450 Enzyme Inhibitors; D004791:Enzyme Inhibitors; D010975:Platelet Aggregation Inhibitors; D058919:Purinergic P2 Receptor Antagonists; D012982:Sodium, Dietary; D014230:Triazoles; C077792:pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid; C033020:1-aminobenzotriazole; D009569:Nitric Oxide; D011732:Pyridoxal Phosphate; D000255:Adenosine Triphosphate; D003577:Cytochrome P-450 Enzyme System; D012964:Sodium; D019331:NG-Nitroarginine Methyl Ester