Submitted to: Medical Science Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/20/1996
Publication Date: N/A
Citation: Interpretive Summary: Prior studies of severely copper-deficient rats have shown that the ability of their blood vessels to dilate is depressed. Such a defect could possibly lead to development of high blood pressure or altered regulation of blood flow. Because humans rarely consume such severely deficient diets, the purpose of the present study was to determine whether rats fed a less severely restricted (marginal) diet suffered the same functional consequences to their blood vessels. For up to five months rats were fed an adequate diet or a marginal diet that contained about one-sixth of their recommended copper intake. The ability of blood vessels from marginally deficient rats to dilate (to a relaxing agent, acetylcholine) was exaggerated in the first two months and depressed in the last three months of the deficiency. Rats did not develop high blood pressure. This study has 1) revealed a previously unobserved exaggerated ability to relax in short-term marginally-deficient blood vessels, 2) indicated that, given sufficient time, a marginally copper-deficient diet will produce a blood vessel defect similar to that in severely deficient rats, and 3) suggested that any tendency for impaired blood vessel activity to cause high blood pressure is compensated for by other physiological mechanisms. This information will be useful to scientists and consumers interested in trace element nutrition affecting the cardiovascular system.
Technical Abstract: Endothelium-dependent dilation was examined in aortas of rats experiencing marginal copper deficiency. Male, weanling Sprague-Dawley rats were fed diets that were copper-adequate (5 ug Cu/g diet) or marginally copper- deficient (1 ug Cu/g diet) for periods ranging from one to five months. At one month intervals, rings of thoracic aorta were isolated from six rats from each dietary group. Aortic rings were contracted with phenylephrine (3x10**-7 M) and the degree of force reduction was measured after successively increasing doses of acetylcholine (10**-9 - 10**-6 M), an endothelium-dependent vasodilator. Marginal copper deficiency was found to increase the vasodilatory response to acetylcholine at months 1 and 2 and to decrease the response at months 3-5. This phasic response reveals an early, previously unobserved defect in copper-deficient blood vessels and indicates that marginal copper deficiency, given time, produces the same result as a severe deficiency.