['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 pO(2) levels and is susceptible to ischaemic damage. It has not been established if ADO induced vasodilatation is modified by salt intake.', '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 micromol/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.', '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.'] Does sodium intake determine the role of adenosine A2 receptors in control of renal medullary perfusion in the rat?