title: Relaxation by urocortin of rat renal arteries: effects of diabetes in males and females.
abstract: 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 N(W)-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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Departamento de Fisiologi;a, Facultad de Medicina, Universidad Autónoma, Arzobispo Morcillo 2, 28029 Madrid, Spain.
authors.forename: Elena
authors.initials: E
authors.lastname: Sanz
authors.forename: Nuria
authors.initials: N
authors.lastname: Fernández
authors.forename: Luis
authors.initials: L
authors.lastname: Monge
authors.forename: Belén
authors.initials: B
authors.lastname: Climent
authors.forename: Godofredo
authors.initials: G
authors.lastname: Diéguez
authors.forename: Angel Luis
authors.initials: AL
authors.lastname: García-Villalón
mesh_terms: D000818:Animals; D018999:Charybdotoxin / Q000494:pharmacology; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005783:Gender Identity; D066298:In Vitro Techniques; D008297:Male; D008469:Meclofenamic Acid / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D026902:Potassium Channel Blockers / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012077:Renal Artery / Q000187:drug effects*; D054832:Urocortins; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D016861:Cyclooxygenase Inhibitors; D026902:Potassium Channel Blockers; D054832:Urocortins; D014665:Vasodilator Agents; D018999:Charybdotoxin; D008469:Meclofenamic Acid; D003346:Corticotropin-Releasing Hormone; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester