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Maternal copper deficiency perpetuates altered vascular function in Sprague-Dawley rat offspring

Published online by Cambridge University Press:  22 February 2010

C. M. Anderson  and
W. T. Johnson
C. M. Anderson*
Affiliation:
College of Nursing, University of North Dakota, Grand Forks, North Dakota, USA
W. T. Johnson*
Affiliation:
USDA ARS Grand Forks Human Nutrition Research Center1,2, Grand Forks, North Dakota, USA
*
*Address for correspondence: Dr C. M. Anderson, College of Nursing, University of North Dakota, 400 Oxford Street, Room 340D, Grand Forks, North Dakota 58202-9025, USA. (E-mails cindyanderson@mail.und.edu, thomas.johnson@ars.usda.gov)
*Address for correspondence: Dr C. M. Anderson, College of Nursing, University of North Dakota, 400 Oxford Street, Room 340D, Grand Forks, North Dakota 58202-9025, USA. (E-mails cindyanderson@mail.und.edu, thomas.johnson@ars.usda.gov)
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Abstract

Little is known about the consequences of maternal copper (Cu) deficiency on the vascular function of offspring or on perpetuation of vascular effects to a second generation. We examined vascular functional responses in mesenteric arteries from Cu-deficient Sprague-Dawley rat dams and from offspring directly exposed to maternal Cu deficiency during development and lactation and perpetuation of the effects in a second generation of offspring. Dams were fed a diet with marginal (1 mg Cu/kg) or adequate (6 mg Cu/kg) Cu for 3 weeks before conception and throughout pregnancy and lactation periods. Half of the first generation (F1) litters were cross-fostered. At reproductive maturity, F1 pairs were bred within groups resulting in second generation (F2) offspring. At 9 weeks of age, mesenteric artery (200 μm) isometric tension was determined in response to vasoconstrictors and vasorelaxants using a small artery wire myograph. Cu deficiency did not alter the vascular function in dams. In F1 offspring, increased responsiveness to potassium chloride in male offspring was due to direct exposure to maternal Cu deficiency in the birth mother, while enhanced endothelium-dependent relaxation responses in female offspring resulted from postnatal exposure to maternal Cu deficiency. Increased endothelium independent and decreased endothelium-dependent relaxation responses were identified in F2 Cu-deficient male offspring. These data indicate that exposure to maternal Cu deficiency during critical windows of development alter the vascular function across two generations of offspring.

Keywords

copper deficiencyfetal programmingnutritionpregnancyvascular function
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 1 , Issue 2 , April 2010 , pp. 131 - 140
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2010

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Footnotes

1

The US Department of Agriculture, Agricultural Research Service, Northern Plains Area, is an equal opportunity/affirmative action employer and all agency services are available without discrimination.

2

Mention of trade names or commercial products in this article is solely to provide specific information and does not imply recommendation or endorsement by the US Department of Agriculture.

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