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Atorvastatin restores endothelial function in offspring of protein restricted rats in a cholesterol-independent manner

Torrens, Christopher, Kelsall, Christopher J., Hopkins, Laura A., Anthony, Frederick W., Curzen, Nick P. and Hanson, Mark A. (2009) Atorvastatin restores endothelial function in offspring of protein restricted rats in a cholesterol-independent manner Hypertension, 53, (4), pp. 661-667. (doi:10.1161/HYPERTENSIONAHA.108.122820).

Record type: Article

Abstract

Maternal protein restriction in rats leads to endothelial dysfunction and decreased NO bioavailability in the offspring. Statins (3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors) are recognized to have pleiotropic actions including increasing NO bioavailability and reducing inflammation and oxidative damage. This study assessed statin treatment on vascular function in a model of endothelial dysfunction, which is independent of dyslipidemia. Wistar rats were fed a control (18% casein) or protein-restricted (9% casein) diet throughout pregnancy. At weaning, a subset of the protein-restricted group was given atorvastatin (10 mg/kg per day) in the drinking water. At 145 days of age, offspring were euthanized by CO2 inhalation. Plasma samples were collected for markers of inflammation, vascular reactivity of the thoracic aorta, and small mesenteric arteries were assessed on the wire myograph, and tissues were snap frozen for molecular biology analysis. Thoracic aorta endothelial-dependent vasodilatation was attenuated in the male offspring from both protein-restricted groups compared with controls (P<0.05) but was similar in females (P value not significant). Endothelial-dependent dilatation of mesenteric arteries was attenuated in male and female protein-restricted offspring (P<0.05) and was corrected by atorvastatin. Maternal protein restriction increased plasma inflammatory markers granulocyte chemotactic protein, lipocalin-2, and ?2-microglobulin in male and C-reactive protein in female offspring (P<0.05). Atorvastatin had no effect on inflammatory markers in the males but restored C-reactive protein to control levels in the females (P<0.05). Aortic and mesenteric artery mRNA levels of endothelial NO synthase, superoxide dismutase 1, and tumor necrosis factor-{alpha} were unchanged. These data suggest that atorvastatin can restore endothelial function in this model, but its effects are gender specific and dependent on the vascular bed

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More information

Published date: 1 April 2009
Keywords: statins, atorvastatin, experimental models, fetal programming, vascular biology, endothelium, nitric oxide, inflammation
Organisations: Dev Origins of Health & Disease

Identifiers

Local EPrints ID: 66508
URI: http://eprints.soton.ac.uk/id/eprint/66508
ISSN: 0194-911X
PURE UUID: 15ce653a-0c5f-46a3-a485-78fb8c501a9f

Catalogue record

Date deposited: 09 Oct 2009
Last modified: 19 Jul 2017 00:24

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Contributors

Author: Christopher J. Kelsall
Author: Laura A. Hopkins
Author: Nick P. Curzen
Author: Mark A. Hanson

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