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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #78396
Title: DIETARY COPPER DEFICIENCY INCREASES TONE IN RESISTANCE ARTERIOLES OF THE RAT

Author
item SCHUSCHKE, D - UNIVERSITY OF LOUISVILLE
item Saari, Jack
item FALCONE, J - UNIVERSITY OF LOUISVILLE
item MILLER, F - UNIVERSITY OF LOUISVILLE

Submitted to: Nutrition International Congress Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 7/27/1997
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Dietary copper restriction has been shown to depress nitric-oxide (NO) mediated vascular smooth muscle relaxation in both aortas and small precapillary arterioles. In the present study we quantitated the effect of copper-deficient diet on vascular tone in resistance arterioles. Male weanling Sprague-Dawley rats were fed purified diets that were either copper-adequate (CuA, 6 ug Cu/g) or copper-deficient (CuD, 0.4 ug Cu/g) for 4 weeks. Rats were anesthetized, then the diameter of the large feeding arterioles (A1) and the branch arterioles (A2) were quantitated before and after maximal dilation with 10**-4 M papaverine. A1 baseline diameters were significantly less in the CuD group (94.8 +/- 7.1 um) than in the CuA group (129.6 +/- 8.1 um) while dilated diameters were not different. In the A2 vessels, there was no difference between groups in either baseline diameters or maximally dilated diameters. Systemic blood pressure and heart rate also did not differ between groups. These result suggest a greater baseline tone in the larger peripheral vascular arterioles of CuD rats which is not present in smaller branches of the arterial tree. We propose that the increased tone in the CuD rats is result of the decreased efficacy of NO which is more important in large arterioles than in smaller ones. The resulting increased peripheral vascular resistance may contribute to the development of systemic hypertension in CuD. Supported by USDA agreement 95-37200-1625.