ArticlePhysiological reports2013
Obese melanocortin-4 receptor-deficient rats exhibit augmented angiogenic balance and vasorelaxation during pregnancy.
Article in Physiological reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 25 citations in OpenAlex.
- Investigating the Impact of Maternal Obesity on Disease Severity in a Mouse Model of Preeclampsia.Nutrients · 2025Article
- Pathophysiology of Maternal Obesity and Hypertension in Pregnancy.Journal of cardiovascular development and disease · 2025Review
- Implications of pregnancy on cardiometabolic disease risk: preeclampsia and gestational diabetes.American journal of physiology. Cell physiology · 2024Review
- Guidelines for in vivo models of developmental programming of cardiovascular disease risk.American journal of physiology. Heart and circulatory physiology · 2024Review
- Significance of the sFlt-1/PlGF Ratio in Certain Cohorts - What Needs to be Considered?Geburtshilfe und Frauenheilkunde · 2024Article
- Performance of sFlt-1/PIGF Ratio for the Prediction of Perinatal Outcome in Obese Pre-Eclamptic Women.Journal of clinical medicine · 2022Article
- Administration of recombinant human placental growth factor decreases blood pressure in obese hypertensive pregnant rats.Journal of hypertension · 2020Article
- Article
- Mutations in MC4R facilitate the angiogenic activity in patients with orbital venous malformation.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- High-fat diet from parental generation exaggerates body and adipose tissue weights in pregnant offspring.PloS one · 2020Article
- Melanocortin-4 Receptor Deficiency Attenuates Placental Ischemia-Induced Hypertension in Pregnant Rats.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Adrenergic receptor blockade attenuates placental ischemia-induced hypertension.Physiological reports · 2018Article
- Obesity and High-Fat Diet Induce Distinct Changes in Placental Gene Expression and Pregnancy Outcome.Endocrinology · 2018Article
- Heme oxygenase-1 is a potent inhibitor of placental ischemia-mediated endothelin-1 production in cultured human glomerular endothelial cells.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Exposure to placental ischemia impairs postpartum maternal renal and cardiac function in rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Role of Nitric Oxide Synthase on Blood Pressure Regulation and Vascular Function in Pregnant Rats on a High-Fat Diet.American journal of hypertension · 2017Article
- Physical Activity, Energy Expenditure, and Defense of Body Weight in Melanocortin 4 Receptor-Deficient Male Rats.Scientific reports · 2016Article
- Placental Growth Factor Administration Abolishes Placental Ischemia-Induced Hypertension.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Review
- Immune Mechanisms Linking Obesity and Preeclampsia.Biomolecules · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
While obesity is a major risk factor for preeclampsia, the mechanisms linking obesity and hypertension during preeclampsia remain unclear. Hypertension in preeclampsia is associated with placental ischemia-induced release of anti-angiogenic soluble fms-like tyrosine kinase (sFlt-1) into the maternal circulation, which antagonizes vascular endothelial growth factor (VEGF) promoting endothelial dysfunction. Haploinsufficiency, defined as loss of one copy of a gene via a mutation, of the melanocortin-4 receptor (MC4R) is the most common cause of monogenetic obesity in humans. The purpose of our study was to determine the effects of genetic obesity on angiogenic balance, endothelial function, and blood pressure in pregnant MC4R+/- and MC4R+/+ rats. At gestational day (GD) 18, body weight and total body fat mass were greater in MC4R+/- than MC4R+/+ rats. On GD 19, plasma sFlt-1 was not significantly different between groups. Interestingly, circulating VEGF was greater in the obese rats with the source being adipose tissue and not the placenta. Wire myography showed in third-order mesenteric arteries that sensitivity (logEC50) to endothelial dependent and nitric oxide donor-induced vasorelaxation was greater in MC4R+/- versus MC4R+/+. Mean arterial blood pressure was similar between groups. In conclusion, under normal pregnant conditions, genetically obese pregnant animals have greater angiogenic balance and dependency of vasorelaxation on nitric oxide signaling protecting against the development of hypertension. However, we speculate that, in the face of reduced uterine perfusion, a rise in circulating placental factors that target and reduce nitric oxide bioavailability exposes the susceptibility of genetically obese animals to greater hypertension in pregnancy.
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