ArticleBiology of reproduction2020
Increased uterine artery blood flow in hypoxic murine pregnancy is not sufficient to prevent fetal growth restriction†.
Article in Biology of reproduction, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- The uteroplacental circulation at high altitude: adaptation and maladaptation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- AMPK function in uterine vasculature and placenta at high altitude.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Article
- A maternal hypoxia mouse model to study the effect of late gestational hypoxia on offspring lung outcomes.Frontiers in physiology · 2025Article
- Preeclampsia: Etiology, Pathophysiology, Risk Factors, Impact and Prevention: A Narrative Review.Iranian journal of public health · 2024Review
- H2S donor GYY4137 mitigates sFlt-1-induced hypertension and vascular dysfunction in pregnant rats†.Biology of reproduction · 2024Article
- Effects of hypoxia on uteroplacental and fetoplacental vascular function during pregnancy.Frontiers in physiology · 2024Review
- Restoring Angiotensin Type 2 Receptor Function Reverses PFOS-Induced Vascular Hyper-Reactivity and Hypertension in Pregnancy.International journal of molecular sciences · 2023Article
- Standardisation and future of preclinical echocardiography.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Review
- Dousing the flame: reviewing the mechanisms of inflammatory programming during stress-induced intrauterine growth restriction and the potential for ω-3 polyunsaturated fatty acid intervention.Frontiers in physiology · 2023Review
- Prenatal Hypoxia Affects Foetal Cardiovascular Regulatory Mechanisms in a Sex- and Circadian-Dependent Manner: A Review.International journal of molecular sciences · 2022Review
- Fetal Cardiac Lipid Sensing Triggers an Early and Sex-related Metabolic Energy Switch in Intrauterine Growth Restriction.The Journal of clinical endocrinology and metabolism · 2021Article
- Placental Ischemia Says "NO" to Proper NOS-Mediated Control of Vascular Tone and Blood Pressure in Preeclampsia.International journal of molecular sciences · 2021Review
- Uteroplacental nutrient flux and evidence for metabolic reprogramming during sustained hypoxemia.Physiological reports · 2021Article
- Activation of angiotensin type 2 receptor attenuates testosterone-induced hypertension and uterine vascular resistance in pregnant rats†.Biology of reproduction · 2021Article
- Enhanced Placental Mitochondrial Respiration in Tibetan Women at High Altitude.Frontiers in physiology · 2021Article
- AMP-activated protein kinase activator AICAR attenuates hypoxia-induced murine fetal growth restriction in part by improving uterine artery blood flow.The Journal of physiology · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Incomplete maternal vascular responses to pregnancy contribute to pregnancy complications including intrauterine growth restriction (IUGR) and preeclampsia. We aimed to characterize maternal vascular dysfunction in a murine model of fetal growth restriction as an approach toward identifying targetable pathways for improving pregnancy outcomes. We utilized a murine model of late-gestation hypoxia-induced IUGR that reduced E18.5 fetal weight by 34%. Contrary to our hypothesis, uterine artery blood flow as measured in vivo by Doppler ultrasound was increased in mice housed under hypobaric hypoxia (385 mmHg; 5500 m) vs normoxia (760 mmHg; 0 m). Using wire myography, uterine arteries isolated from hypoxic mice had similar vasodilator responses to the two activators A769662 and acetylcholine as those from normoxic mice, although the contribution of an increase in nitric oxide production to uterine artery vasodilation was reduced in the hypoxic vs normoxic groups. Vasoconstrictor responses to phenylephrine and potassium chloride were unaltered by hypoxia. The levels of activated adenosine monophosphate-activated protein kinase (AMPK) were reduced with hypoxia in both the uterine artery and placenta as measured by western blot and immunohistochemistry. We concluded that the rise in uterine artery blood flow may be compensatory to hypoxia but was not sufficient to prevent fetal growth restriction. Although AMPK signaling was reduced by hypoxia, AMPK was still receptive to pharmacologic activation in the uterine arteries in which it was a potent vasodilator. Thus, AMPK activation may represent a new therapy for pregnancy complications involving reduced uteroplacental perfusion.
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Registered trials
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