|Schuschke, Dale - UNIVERSITY OF LOUISVILLE|
|Falcone, Jeff - UNIVERSITY OF LOUISVILLE|
Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: November 10, 2006
Publication Date: April 1, 2007
Repository URL: http://www.fasebj.org
Citation: Schuschke, D.A., Johnson, W.T., Falcone, J.C. 2007. Copper deficiency attenuates endothelial nitric oxide release [abstract]. Journal of Federation of American Societies for Experimental Biology.21(5):A721. Technical Abstract: The attenuation of endothelium-dependent nitric oxide (NO)-mediated vasodilation is a consistent finding in both conduit and resistance vessels during dietary copper deficiency. While the effect is well established, evidence for the mechanism is still circumstantial. This study was designed to determine the amount of NO released from the vascular endothelium. Using the fluorescent NO indicator, DAF-FM, we now report the effect of a copper-deficient diet on NO release from the endothelium of resistance arterioles. Weanling Sprague-Dawley rats were fed purified diets which were either copper-adequate (CuA; 6.3 ug Cu/g diet) or copper-deficient (CuD; 0.3ug Cu/g diet) for 4 weeks. First-order arterioles were microsurgically isolated from the rat cremaster muscle, cannulated and pressurized with MOPS-PSS. DAF-FM (5uM) was added in the lumen of the vessel and the pressure was maintained at -3 mmHg to prevent an increase in luminal diameter and dilution of the dye. In response to 10**-6 M Ach, fluorescent intensity significantly increased from baseline in the CuA group while there was no significant change in the CuD group. These results correspond with our previous data showing a significant mobilization of Ca**++ to Ach in CuA but not CuD arterioles. The results suggest that production of NO by the vascular endothelium is inhibited by a dietary restriction of copper. This inhibition may account for the attenuated vasodilation previously reported in CuD rats. Supported by NIH DK055030.