Horm Metab Res 1998; 30(1): 55-57
DOI: 10.1055/s-2007-978831
Original Clinical

© Georg Thieme Verlag Stuttgart · New York

Decreased Endothelium Dependent Relaxation (Nitric Oxide) in Diabetic Kidneys

A. Costa e Forti1 , 2 , M. C. Fonteles2
  • 1Department of Clinical Medicine, Federal University of Ceará, Fortaleza, CE
  • 2Clinical Research Unit, Federal University of Ceará, Fortaleza, CE
Further Information

Publication History



Publication Date:
20 April 2007 (online)

To evaluate the endothelium-dependent vasodilatation in diabetic kidneys, we have perfused rabbit kidneys at 30°C with Krebs-Henseleit solution in a non-recirculated perfusion system. To increase vascular tonus, we infused norepinephrine (NOR) (10-6 M) into the renal artery. After the vasoconstriction reached steady state conditions, a dose-response study was performed with acetylcholine (Ach) and bradykinin (Bk). Administration of Ach (10-7 M - 10-5 M) or Bk (10-8 - 10-7 M) in cumulative curves through the renal artery promoted a vasodilation, which was dose-dependent in normal and diabetic (three weeks after 150 mg of alloxan, intraperitoneally) kidney. We found a decreased vasodilator response to Ach (p<0.05) and Bk (p<0.01) in diabetic animals, when compared to controls. When sodium nitroprusside (10-8 - 10-7 M) was administrated through the renal artery to evaluate the endothelium-independent vasodilating effects, a similar vasodilator response was found in both normal and diabetic kidneys. These data indicate for a failure of the vasodilator mechanism dependent on endothelium in alloxan-diabetic kidneys.