title: Maternal salt and fat intake causes hypertension and sustained endothelial dysfunction in fetal, weanling and adult male resistance vessels.
abstract: 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.
authors.affiliation: Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, New Zealand.
authors.forename: Clint
authors.initials: C
authors.lastname: Gray
authors.affiliation: Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, New Zealand.
authors.forename: Claudia J
authors.initials: CJ
authors.lastname: Harrison
authors.affiliation: Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, New Zealand.
authors.forename: Stephanie A
authors.initials: SA
authors.lastname: Segovia
authors.affiliation: Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, New Zealand.
authors.forename: Clare M
authors.initials: CM
authors.lastname: Reynolds
authors.affiliation: Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, New Zealand.
authors.forename: Mark H
authors.initials: MH
authors.lastname: Vickers
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004032:Diet / Q000009:adverse effects*; D004041:Dietary Fats; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D006439:Hemodynamics / Q000187:drug effects; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D018811:Maternal Exposure; D010656:Phenylephrine / Q000494:pharmacology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011453:Prostaglandins / Q000378:metabolism; D012333:RNA, Messenger; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction; D017673:Sodium Chloride, Dietary; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D004041:Dietary Fats; D011453:Prostaglandins; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D017673:Sodium Chloride, Dietary; D014665:Vasodilator Agents; D010656:Phenylephrine; D000109:Acetylcholine