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Maternal salt and fat intake causes hypertension and sustained endothelial dysfunction in fetal, weanling and adult male resistance vessels
Maternal salt and fat intake can independently programme adult cardiovascular status, increasing risk of cardiovascular disease in offspring. Despite its relevance to modern western-style dietary habits, the interaction between increased maternal salt and fat intake has not been examined. Female vir...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4424661/ https://www.ncbi.nlm.nih.gov/pubmed/25953742 http://dx.doi.org/10.1038/srep09753 |
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author | Gray, Clint Harrison, Claudia J. Segovia, Stephanie A. Reynolds, Clare M. Vickers, Mark H. |
author_facet | Gray, Clint Harrison, Claudia J. Segovia, Stephanie A. Reynolds, Clare M. Vickers, Mark H. |
author_sort | Gray, Clint |
collection | PubMed |
description | Maternal salt and fat intake can independently programme adult cardiovascular status, increasing risk of cardiovascular disease in offspring. Despite its relevance to modern western-style dietary habits, the interaction between increased maternal salt and fat intake has not been examined. Female virgin Sprague-Dawley rats were fed, a standard control diet (CD) (10% kcal fat, 1% NaCl), High-fat diet (HF) (45% kcal fat, 1% NaCl), High-salt diet (SD) (10% kcal fat, 4% NaCl), High-fat high-salt diet (HFSD) (45% kcal fat, 4% NaCl) prior to pregnancy, during pregnancy and throughout lactation. Fetal, weanling and adult vessels were mounted on a pressure myograph at fetal day 18, weaning day 21 and day 135 of adulthood. Increased blood pressure in SD, HFD and HFSD male offspring at day 80 and 135 of age was consistent with perturbed vascular function in fetal, weanling and adult vessels. Maternal salt intake reduced EDHF and calcium-mediated vasodilation, maternal fat reduced NO pathways and maternal fat and salt intake, a combination of the two pathways. Adult offspring cardiovascular disease risk may, in part, relate to vascular adaptations caused by maternal salt and/or fat intake during pregnancy, leading to persistent vascular dysfunction and sustained higher resting blood pressure throughout life. |
format | Online Article Text |
id | pubmed-4424661 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-44246612015-05-13 Maternal salt and fat intake causes hypertension and sustained endothelial dysfunction in fetal, weanling and adult male resistance vessels Gray, Clint Harrison, Claudia J. Segovia, Stephanie A. Reynolds, Clare M. Vickers, Mark H. Sci Rep Article Maternal salt and fat intake can independently programme adult cardiovascular status, increasing risk of cardiovascular disease in offspring. Despite its relevance to modern western-style dietary habits, the interaction between increased maternal salt and fat intake has not been examined. Female virgin Sprague-Dawley rats were fed, a standard control diet (CD) (10% kcal fat, 1% NaCl), High-fat diet (HF) (45% kcal fat, 1% NaCl), High-salt diet (SD) (10% kcal fat, 4% NaCl), High-fat high-salt diet (HFSD) (45% kcal fat, 4% NaCl) prior to pregnancy, during pregnancy and throughout lactation. Fetal, weanling and adult vessels were mounted on a pressure myograph at fetal day 18, weaning day 21 and day 135 of adulthood. Increased blood pressure in SD, HFD and HFSD male offspring at day 80 and 135 of age was consistent with perturbed vascular function in fetal, weanling and adult vessels. Maternal salt intake reduced EDHF and calcium-mediated vasodilation, maternal fat reduced NO pathways and maternal fat and salt intake, a combination of the two pathways. Adult offspring cardiovascular disease risk may, in part, relate to vascular adaptations caused by maternal salt and/or fat intake during pregnancy, leading to persistent vascular dysfunction and sustained higher resting blood pressure throughout life. Nature Publishing Group 2015-05-08 /pmc/articles/PMC4424661/ /pubmed/25953742 http://dx.doi.org/10.1038/srep09753 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Gray, Clint Harrison, Claudia J. Segovia, Stephanie A. Reynolds, Clare M. Vickers, Mark H. Maternal salt and fat intake causes hypertension and sustained endothelial dysfunction in fetal, weanling and adult male resistance vessels |
title | Maternal salt and fat intake causes hypertension and sustained endothelial dysfunction in fetal, weanling and adult male resistance vessels |
title_full | Maternal salt and fat intake causes hypertension and sustained endothelial dysfunction in fetal, weanling and adult male resistance vessels |
title_fullStr | Maternal salt and fat intake causes hypertension and sustained endothelial dysfunction in fetal, weanling and adult male resistance vessels |
title_full_unstemmed | Maternal salt and fat intake causes hypertension and sustained endothelial dysfunction in fetal, weanling and adult male resistance vessels |
title_short | Maternal salt and fat intake causes hypertension and sustained endothelial dysfunction in fetal, weanling and adult male resistance vessels |
title_sort | maternal salt and fat intake causes hypertension and sustained endothelial dysfunction in fetal, weanling and adult male resistance vessels |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4424661/ https://www.ncbi.nlm.nih.gov/pubmed/25953742 http://dx.doi.org/10.1038/srep09753 |
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