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Cardiovascular Research 2003 58(3):706-711; doi:10.1016/S0008-6363(03)00293-1
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Relaxation by urocortin of rat renal arteries: effects of diabetes in males and females

Elena Sanz, Nuria Fernández, Luis Monge, Belén Climent, Godofredo Diéguez and Angel Luis García-Villalón*

Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Arzobispo Morcillo 2, 28029 Madrid, Spain

angeluis.villalon{at}uam.es

* Corresponding author. Tel.: +34-91-397-5412; fax: +34-91-397-5324.

Objective: Urocortin is a peptide structurally related to corticotropin releasing factor (CRF), and the present study was performed to examine the effects of diabetes mellitus on the relaxation by urocortin of renal arteries from males and females. Methods: The response to urocortin was studied in isolated segments, 2 mm long, from renal arteries, from male and female, control (normoglycemic) and streptozotocin-induced diabetic rats. Results: In the renal arterial segments precontracted with endothelin-1, urocortin produced concentration-dependent relaxation, that was not different between males and females. Diabetes reduced the relaxation in renal arteries from females but not in those from males. The potassium channel blocker charybdotoxin (10–7 M) reduced the relaxation to urocortin of renal arteries from normoglycemic males and females. The cyclooxygenase inhibitor meclofenamate did not modify the relaxation to urocortin in renal arteries from normoglycemic males or females. The inhibitor of nitric oxide synthesis NW-nitro-L-arginine methyl ester (L-NAME, 10–4 M) reduced the relaxation to urocortin in renal arteries from normoglycemic females, but not in renal arteries from normoglycemic males. Neither charybdotoxin, L-NAME or meclofenamate modified the relaxation to urocortin of renal arteries from diabetic females. Conclusion: These results suggest that urocortin produces a marked vasodilation of renal arteries, which may be mediated by nitric oxide in females and by activation of potassium channels in both genders, and is reduced by diabetes in renal arteries from females.

KEYWORDS Diabetes; Gender; K-channel; Renal function; Vasoconstriction/dilation


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