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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 #107267
Title: DIETARY COPPER DEFICIENCY REDUCES THE ELEVATION OF BLOOD PRESSURE CAUSED BY NITRIC OXIDE SYNTHASE INHIBITION

Author
item Saari, Jack

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/10/1999
Publication Date: 3/15/2000
Citation: Saari, J.T. 2000. Dietary copper deficiency reduces the elevation of blood pressure caused by nitric oxide synthase exhibition [abstract]. The Federation of American Societies for Experimental Biology Journal. 15:A773.

Interpretive Summary:

Technical Abstract: Nitric oxide (NO)-mediated vasodilation is reduced in isolated aortas and in bathed microcirculatory preparations from copper (Cu)-deficient rats. A possible consequence, elevated blood pressure, has been observed, but is not a consistent finding. Our objective was to determine whether Cu deficiency affects blood pressure regulation via an effect on NO. Twenty- four male weanling rats were given diets that contained 0.4, 0.8, 2.5 or 7.2 mg Cu/kg diet. After 5 wks each rat was anesthetized and their right carotid artery and jugular vein were cannulated. Blood pressure was measured via the carotid artery before and after injection into the jugular vein of the NO synthase inhibitor, (L-NAME, 10 mg/kg body wt). The varied dietary Cu intakes produced a wide range of liver Cu concentration (22-241 nmol/g), against which blood pressure, before and after L-NAME injection, was plotted. Control mean arterial blood pressure (MAP; range, 104-152 mm Hg) was not correlated with liver Cu concentration (r=0.12 , p>0.05). However, both the MAP after L-NAME treatment (MAPl, range 148-190 mm Hg) and the elevation of MAP caused by L-NAME (delta MAP; range, 8-68 mm Hg) were greater in Cu-adequate than in Cu-deficient rats, as indicated by significant positive correlations with liver Cu concentration (r=0.52 for MAPl; r=0.42 for delta MAP; p<0.05). This suggests that NO plays a significant role in maintaining basal blood pressure in Cu-adequate rats that is reduced by Cu deficiency. This is consistent with the reduced NO-mediated responses observed in isolated vessels and microcirculation of Cu-deficient animals. Further study is required to determine the compensatory factor that maintains basal blood pressure in Cu-deficient rats in the relative absence of control by NO.