Background: The precise mechanisms regulating the natriuretic peptide urodilatin (ANP-95-126) remain to be defined. Renal excretion of urodilatin (UUROV) has been shown to be modified by variations in plasma sodium and renal perfusion pressure. This suggests a relationship between urodilatin and the renin-angiotensin system. Methods: We investigated the effects of angiotensin II (AII, 0.1 nmol/l) and the AT1 receptor antagonist losartan (LS, 1 µmol/l) on UUROV and renal function in isolated rat kidneys perfused for 180 min in a closed circuit system. A further series employing a vasoconstricting concentration of endothelin-1 (ET-1, 0.01 nmol/l) was performed to explore the effects of vasoconstriction and glomerular filtration rate (GFR) on UUROV. Results: Urine flow (UV) and urinary sodium excretion (UNaV) decreased and renal vascular resistance (RVR) increased after treatment with AII (n = 5) in comparison with a control group (n = 6; p < 0.05). Treatment with LS (n = 5) and AII+LS (n = 5) had no significant effect on these parameters. GFR decreased after AII (p < 0.05) and was not significantly altered by other interventions. UUROV decreased after AII (p < 0.05) and was comparable to the control group after LS and AII+LS. ET-1 (n = 5) induced a significant increase in RVR and decreased UV and UNaV (p < 0.05). Point-to-point analysis revealed that the ET-1-induced vasoconstriction and the subsequent decrease in GFR had no effect on UUROV. Conclusions: This suggests that vasoconstrictory concentrations of AII decrease UUROV in the isolated perfused rat kidney. The lack of effect of ET-1 on UUROV suggests that the AII-induced alterations in urodilatin excretion cannot be explained by vasoconstriction per se.

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