Vasodilation to Vascular Endothelial Growth Factor in the Uterine Artery of the Pregnant Rat Is Blunted by Low Dietary Protein Intake

Itoh, Shigeru; Brawley, L; Wheeler, T.; Anthony, F.W.; Poston, Lucilla; Hanson, Mark A.

doi:10.1203/00006450-200204000-00014

Cited by 60 publications

(65 citation statements)

References 33 publications

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“…6 In the present study, we have repeated that observation and demonstrated that supplementing the maternal diet with folate restores VEGF-induced dilatation of the uterine artery. This folate-induced restoration of maternal vasodilatation is most likely mediated through changes in the NO pathway.…”

Section: Discussionsupporting

confidence: 76%

“…6 Cumulative concentration response curves (CRCs) were measured for phenylephrine (PE, 1 nM to 100 mol/L). Then, after preconstriction with PE (EC 80 ), cumulative CRCs to acetylcholine (ACh, 1 nM to 10 mol/L), vascular endothelial growth factor (VEGF; 10 pM to 3 nM), isoprenaline (ISO, 1 nM to 30 mol/L), calcitonin gene-related peptide (CGRP; 1 pm to 3 nM), and adrenomedullin (ADM, 1 pM to 30 nM) were conducted.…”

Section: Vascular Protocol: Maternal Uterine Arteriesmentioning

confidence: 99%

“…6 It remains possible, therefore, that alterations occur in different cell signaling pathways in different arterial beds, and perhaps, therefore, the defect lies not in NO production but rather the cAMP pathway. The main component of ISO-induced vasodilatation is the activation of adenylate cyclase producing a subsequent rise in cAMP.…”

Section: Torrens Et Al Folate Prevents Offspring Vascular Defectsmentioning

confidence: 99%

“…4 The offspring phenotype induced by such dietary manipulation has similarities with the human metabolic syndrome, providing further evidence for a developmental component to the etiology of this syndrome and giving models for investigating the underlying mechanisms. 5 In the rat, we have demonstrated previously that maternal protein restriction during pregnancy leads to impaired endothelial function in the uterine and mesenteric arteries of the dam in late pregnancy 6 and that supplementation of the maternal diet with glycine reverses this effect. 7 An adequate supply of dietary folate in early pregnancy has long been recognized to be necessary for normal embryo development, and supplementation lowers the incidence of congenital defects.…”

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Folate Supplementation During Pregnancy Improves Offspring Cardiovascular Dysfunction Induced by Protein Restriction

et al. 2006

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Abstract-Dietary protein restriction in the rat compromises the maternal cardiovascular adaptations to pregnancy and leads to raised blood pressure and endothelial dysfunction in the offspring. In this study we have hypothesized that dietary folate supplementation of the low-protein diet will improve maternal vascular function and also restore offspring cardiovascular function. Pregnant Wistar rats were fed either a control (18% casein) or protein-restricted (9% casein) diet Ϯ5 mg/kg folate supplement. Function of isolated maternal uterine artery and small mesenteric arteries from adult male offspring was assessed, systolic blood pressure recorded, and offspring thoracic aorta levels of endothelial nitric oxide (NO) synthase mRNA measured. In the uterine artery of late pregnancy dams, vasodilatation to vascular endothelial growth factor was attenuated in the protein-restricted group but restored with folate supplementation, as was isoprenaline-induced vasodilatation (PϽ0.05). In male offspring, protein restriction during pregnancy led to raised systolic blood pressure (PϽ0.01), impaired acetylcholine-induced vasodilatation (PϽ0.01), and reduced levels of endothelial NO synthase mRNA (PϽ0.05). Maternal folate supplementation during pregnancy prevented this elevated systolic blood pressure associated with a protein restriction diet. With folate supplementation, endothelium-dependent vasodilatation and endothelial NO synthase mRNA levels were not significantly different from either the control or protein-restricted groups. Maternal folate supplementation of the control diet had no effect on blood pressure or vasodilatation. This study supports the hypothesis that folate status in pregnancy can influence fetal development and, thus, the risks of cardiovascular disease in the next generation. The concept of developmental origins of adult disease focuses predominately on fetal life but must also include a role for maternal cardiovascular function. Key Words: diet Ⅲ endothelium Ⅲ hypertension, experimental Ⅲ nitric oxide Ⅲ pregnancy C ardiovascular disease arises from complex interactions between genetic susceptibility and adverse environmental influences. Increasing evidence suggests that environmental, particularly nutritional, factors operate from the earliest stages of development. 1,2 The concept of developmental origins of adult disease 3 has been strengthened by observations in animals that an unbalanced diet in pregnancy leads to cardiovascular and metabolic dysfunction in the offspring. 4 The offspring phenotype induced by such dietary manipulation has similarities with the human metabolic syndrome, providing further evidence for a developmental component to the etiology of this syndrome and giving models for investigating the underlying mechanisms. 5 In the rat, we have demonstrated previously that maternal protein restriction during pregnancy leads to impaired endothelial function in the uterine and mesenteric arteries of the dam in late pregnancy 6 and that supplementation of the maternal diet with glycine ...

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Section: Discussionsupporting

confidence: 76%

Section: Vascular Protocol: Maternal Uterine Arteriesmentioning

confidence: 99%

Section: Torrens Et Al Folate Prevents Offspring Vascular Defectsmentioning

confidence: 99%

mentioning

confidence: 95%

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Folate Supplementation During Pregnancy Improves Offspring Cardiovascular Dysfunction Induced by Protein Restriction

et al. 2006

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“…(29). Mean internal diameter was similar in both groups at each time (C-87, 268 Ϯ 9 m, n ϭ 8; PR-87, 269 Ϯ 7 m, n ϭ 9, p Ͼ 0.05; C-164, 274 Ϯ 10 m, n ϭ 9; PR-164, 259 Ϯ 9 m, n ϭ 8, p Ͼ 0.05).…”

Section: Methodsmentioning

confidence: 77%

Dietary Protein Restriction in Pregnancy Induces Hypertension and Vascular Defects in Rat Male Offspring

et al. 2003

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Non‐genomic transgenerational inheritance of disease risk

2007

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That there is a heritable or familial component of susceptibility to chronic non-communicable diseases such as type 2 diabetes, obesity and cardiovascular disease is well established, but there is increasing evidence that some elements of such heritability are transmitted non-genomically and that the processes whereby environmental influences act during early development to shape disease risk in later life can have effects beyond a single generation. Such heritability may operate through epigenetic mechanisms involving regulation of either imprinted or non-imprinted genes but also through broader mechanisms related to parental physiology or behaviour. We review evidence and potential mechanisms for non-genomic transgenerational inheritance of 'lifestyle' disease and propose that the 'developmental origins of disease' phenomenon is a maladaptive consequence of an ancestral mechanism of developmental plasticity that may have had adaptive value in the evolution of generalist species such as Homo sapiens.

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Vasodilation to Vascular Endothelial Growth Factor in the Uterine Artery of the Pregnant Rat Is Blunted by Low Dietary Protein Intake

Cited by 60 publications

References 33 publications

Folate Supplementation During Pregnancy Improves Offspring Cardiovascular Dysfunction Induced by Protein Restriction

Folate Supplementation During Pregnancy Improves Offspring Cardiovascular Dysfunction Induced by Protein Restriction

Dietary Protein Restriction in Pregnancy Induces Hypertension and Vascular Defects in Rat Male Offspring

Non‐genomic transgenerational inheritance of disease risk

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