@misc{Kuczeriszka_Marta_Adenosine_2013,
 author={Kuczeriszka, Marta and Dobrowolski, Leszek and Walkowska, Agnieszka and Sadowski, Janusz and Kompanowska-Jezierska, Elżbieta},
 editor={Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland},
 copyright={Rights Reserved - Restricted Access},
 address={Basel},
 howpublished={online},
 year={2013},
 language={eng},
 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},
 type={Text},
 title={Adenosine effects on renal functionin the rat: role of sodium intake and cytochrome P450},
 volume={123},
 number={1-2},
 journal={Nephron Physiology},
 publisher={Karger},
 keywords={Adenosine, Sodium intake, Kidney -- Physiology, Adenosine--analogs & derivatives, Renal Circulation--physiology},
}