ObjectivesTo investigate the effects of the interaction between adenosine receptors and renal nerves on urinary sodium excretion and glomerular filtration rate.Methods and designThe effects on water and sodium excretion and glomerular filtration rate of A1 [2-chloro-N6-cyclopentyl-adenosine (CCPA)] and A2 [2-hesinyl-5′-N-ethyl-carboxamido-adenosine (2HE-NECA)] adenosine agonists were studied in anaesthetized rats with one kidney surgically denervated. Arterial blood pressure, heart rate and rate of urine flow from each kidney were continuously recorded; inulin clearance was used as an index of glomerular filtration rate. The experiments were performed with three groups of rats, into which, after a control period of 20 min, CCPA, 2HE-NECA or vehicle was infused for two subsequent 20 min periods.ResultDuring infusion of CCPA, the slight decrease in arterial pressure was associated with a transient decrease in glomerular filtration rate and marked long-lasting decreases in heart rate, water and sodium excretion and fractional sodium excretion. The response of the innervated kidney was similar to the response of the denervated kidney. Infusion of 2HE-NECA caused decreases in arterial pressure, glomerular filtration rate and excretion of water and sodium associated with an increase in heart rate. The reduction of water and sodium excretion from the innervated kidney was larger than that from the denervated kidney.ConclusionsActivation both of A1 and of A2 receptor causes a reduction in urinary water and sodium excretion. The renal response to activation of A2 receptors is enhanced by the presence of renal nerves, whereas the response to activation of A1 receptors is not influenced by renal nerves.