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1 Maternal and Fetal Research Unit, Division of Reproductive Health, Endocrinology and Development, King's College London, London, UK
2 Faculty of Life Sciences, University of Manchester, Manchester, UK
3 Stereological Research and Electron Microscopy Laboratory, University of Aarhus, Aarhus, Denmark
Evidence from human and animal studies suggests that maternal nutrition can induce developmental programming of adult hypertension in offspring. We have previously described a model of maternal dietary imbalance in Sprague-Dawley rats whereby administration of a maternal diet rich in animal lard programmes the development of increased blood pressure, insulin resistance, dyslipidaemia, obesity and mesenteric artery endothelial dysfunction in adult offspring. To further characterize the mechanism of hypertension in this model we have examined vascular and renal structure in adult offspring of Sprague-Dawley rats fed a control diet (OC) or lard-rich diet (OHF) during pregnancy and suckling followed by a control diet post-weaning. To gain further insight, we assessed aortic reactivity and elasticity in an organ bath preparation and renal renin and Na+,K+-ATPase activity. Plasma aldosterone concentration was also measured. Stereological examination of the aorta in OHF demonstrated reduced endothelial cell volume and smooth muscle cell number compared with OC. Adult OHF animals showed increased aortic stiffness and reduced endothelium-dependent relaxation. Renal stereology showed no differences in kidney weight, glomerular number or volume in OHF compared with OC, but renin and Na+,K+-ATPase activity were significantly reduced in OHF compared with controls. Programmed alterations to aortic structure and function are consistent with previous observations that exposure to maternal high fat diets produces systemic vascular changes in the offspring. Despite normal renal stereology, altered renal Na+,K+-ATPase and renin activity offers further insight into the mechanism underlying the increased blood pressure characteristic of this model.
(Received 11 February 2005;
accepted after revision 10 March 2005;
first published online 17 March 2005)
Corresponding author J. A. Armitage: Maternal and Fetal Research Unit, Division of Reproductive Health, Endocrinology and Development, GKT Department of Women's Health, 10th Floor, North Wing, St Thomas' Hospital, Lambeth Palace Road, London SE1 7EH, UK. Email: james.armitage{at}kcl.ac.uk
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