Search for: [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"]

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