Inhibitory effect of iron on vasodilatation in the isolated rat aorta

AIM: The objectives of the present study were to examine the effect of iron on relaxation of isolated rat aortic rings, and to elucidate the underlying mechanism. METHODS: The thoracic aortic rings of male Sprague-Dawley rats were mounted on bath system. Vasodilatation of aortic rings preconstricted with 10^-6 mol/L of phenylephrine (PE) was measured. RESULTS: (1) Exposure of endothelium-intact aortic rings to ferric ammonium citrate (FAC) for 30 min caused a significant reduction in the relaxation response to acetylcholine (ACh). Pretreatment with L-arginine (L-Arg) before incubation with FAC did not reverse the inhibition of relaxation response to ACh completely. (2) In endothelium-intact aortic rings, L-Arg relaxed the PE preconstricted vessels. Exposure to FAC for 30 min caused the decrease in the relaxation response to L-Arg. There was no difference in the relaxation response to nitric oxide donor, sodium nitroprusside, between endothelium-denuded arteries treated with or without FAC. (3) Dimethyl sulfoxide had no effect on the inhibition of relaxation to ACh by FAC in endothelium-intact rings. Pretreatment of arteries with glutathione and catalase prevented the decrease in relaxation responses to ACh induced by FAC. (4) The nitric oxide synthase activity was (56.49±2.49)×10³U/g protein in normal aorta with endothelium, while after incubation with FAC for 30 min, it reduced to (25.15±5.75)×10³U/g protein ( P< 0.05). CONCLUSION: Inactivation of nitric oxide synthase and decrease in intracellular glutathione level might mediate iron-induced inhibition of arterial relaxation responses to ACh.