Decreased endothelium dependent relaxation (nitric oxide) in diabetic kidneys.

To evaluate the endothelium-dependent vasodilatation in diabetic kidneys, we have perfused rabbit kidneys at 30 degrees 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.