ArticleThe Journal of physiology2008
Endothelial dysfunction and reduced antioxidant protection in an animal model of the developmental origins of cardiovascular disease.
Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 56 citations in OpenAlex.
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- Sex and Racial Disparities in Peripheral Artery Disease.Arteriosclerosis, thrombosis, and vascular biology · 2023Review
- Assessment of Cardiovascular Health of Children Ages 6 to 10 Years Conceived by Assisted Reproductive Technology.JAMA network open · 2021Article
- Arginine and Endothelial Function.Biomedicines · 2020Review
- Early Life Oxidative Stress and Long-Lasting Cardiovascular Effects on Offspring Conceived by Assisted Reproductive Technologies: A Review.International journal of molecular sciences · 2020Review
- Gender difference in oxidative stress: a new look at the mechanisms for cardiovascular diseases.Journal of cellular and molecular medicine · 2017Review
- Cardiovascular and skeletal muscle ageing: consequences for longevity.The Journal of physiology · 2016Article
- Particulate matter, the newborn methylome, and cardio-respiratory health outcomes in childhood.Environmental epigenetics · 2016Article
- The Programming Power of the Placenta.Frontiers in physiology · 2016Review
- Long Lasting Microvascular Tone Alteration in Rat Offspring Exposed In Utero to Maternal Hyperglycaemia.PloS one · 2016Article
- Arterial endothelial methylome: differential DNA methylation in athero-susceptible disturbed flow regions in vivo.BMC genomics · 2015Article
- The reduction of aorta histopathological images through inhibition of reactive oxygen species formation in hypercholesterolemia rattus norvegicus treated with polysaccharide peptide of Ganoderma lucidum.Iranian journal of basic medical sciences · 2015Article
- Early developmental conditioning of later health and disease: physiology or pathophysiology?Physiological reviews · 2014Review
- Prenatal development is linked to bronchial reactivity: epidemiological and animal model evidence.Scientific reports · 2014Article
- Article
- Pregnancy Complications and Later Development of Hypertension.Current cardiovascular risk reports · 2013Article
- In utero oxidative stress epigenetically programs antioxidant defense capacity and adulthood diseases.Antioxidants & redox signaling · 2012Review
- Interaction between maternal and offspring diet to impair vascular function and oxidative balance in high fat fed male mice.PloS one · 2012Article
- Compensatory feto-placental upregulation of the nitric oxide system during fetal growth restriction.PloS one · 2012Article
- Chronic hyperhomocysteinemia causes vascular remodelling by instigating vein phenotype in artery.Archives of physiology and biochemistry · 2011Article
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6 authors at 2 institutions in 1 country.
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Abstract
Endothelial dysfunction underlies cardiovascular disease (CVD) in humans and is reported in animal models of developmental origins of such disease. We have investigated whether impaired antioxidant defences and NO generation underlie the genesis of endothelial dysfunction and operate as part of the normal processes of developmental plasticity regulating the induction of phenotype in the offspring. Female Wistar rats were fed either a control (C, 18% protein) or protein-restricted (PR, 9% protein) diet throughout pregnancy. Dams and pups were returned to standard laboratory chow post partum. In male offspring, PR resulted in a reduced endothelial responsiveness to acetylcholine (P < 0.05) in resistance arteries, with vascular remodelling evident from a reduction in smooth muscle content. mRNA expression of endothelial NO synthase (eNOS) was increased (P < 0.05) but there was no change in mRNA levels of manganese superoxide dismutase (MnSOD) or glutamate cysteine ligase (GCL) expression. Interestingly, expression of the antioxidant enzyme haem oxygenase-1 (HO-1) was reduced in the liver (P < 0.05). Female PR offspring also showed a reduced endothelial responsiveness but exhibited no changes in expression of eNOS, iNOS, soluble guanylate cyclase (sGC) or antioxidant genes. Thus, in this model of the developmental origins of CVD, the structure and function of resistance arteries in offspring is altered in complex ways which cannot simply be explained by attenuation in vascular eNOS or in antioxidant protection afforded by GCL or MnSOD. The dysfunction in male offspring may partially be counteracted by an up-regulation of eNOS expression; however, PR does lead to reduced HO-1 expression in these offspring, which may affect both their growth and vascular function. Our findings have established that PR induces significant phenotypic changes in male offspring that may be indicative of an adaptive response during development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.