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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 #97422
Title: ACETLYCHOLINE-INDUCED ENDOTHELIAL CELL CALCIUM MOBILIZATION IS REDUCED IN COPPER-DEFICIENT RAT

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

Submitted to: Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 4/17/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Dietary copper deficiency significantly attenuates nitric oxide (NO)-mediated vascular smooth muscle relaxation. There is evidence for both increased inactivation of the NO radical by superoxide, and oxidative damage to the endothelium where NO is produced. We hypothesized that the oxidative stress would disrupt the NO synthetic pathway in the endothelium during copper deficiency. Male weanling rats were fed a copper- adequate (CuA, 6.4 mg Cu/kg diet) or copper-deficient (CuD, 0.4 mg Cu/kg diet) diet for four weeks. Isolated cremaster muscle arterioles (~100um diameter) were used in the study. Western blot analysis of the endothelial nitric oxide synthase (eNOS) concentration did not show a difference between dietary groups. Acetylcholine (Ach)-induced vasodilation was significantly reduced in the CuD group both before and after pretreatment with the eNOS substrate L-arginine. Mobilization of endothelial intracellular calcium ([Ca**2+ ]i as measured by fura-2 fluorescence) in response to 10**-6 M Ach was significantly inhibited in the CuD rats. Coincident with the inhibition of both the change in [Ca**2+ ]i and vasodilation was a depression of vascular Cu/Zn-SOD activity. These data suggest that endothelial Ca**2+ signaling and NO-mediated vascular dilation are likely reduced by increased oxidative damage in copper- deficient rats. Supported by USDA agreement 95-37200-1625.