ArticleJournal of the American Heart Association2017
Prenatal Hypoxia Induced Dysfunction in Cerebral Arteries of Offspring Rats.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- GDM enhanced acetylcholine induced vasoconstriction in human umbilical vein via CHRM3 and CACNA1C upregulation linked to promoter hypomethylation.Scientific reports · 2025Article
- Gating Mechanism for Biased Agonism at Angiotensin II Type 1 Receptors.Molecules (Basel, Switzerland) · 2025Article
- Sex-specific differences in the mechanisms for enhanced thromboxane ABiology of sex differences · 2024Article
- Paternal preconception alcohol consumption increased Angiotensin II-mediated vasoconstriction in male offspring cerebral arteries via oxidative stress-AT1R pathway.Addiction biology · 2024Article
- Perinatal Fat-Diets Increased Angiotensin II-Mediated CaNutrients · 2023Article
- Prenatal Hypoxia Affects Foetal Cardiovascular Regulatory Mechanisms in a Sex- and Circadian-Dependent Manner: A Review.International journal of molecular sciences · 2022Review
- Antenatal Hypoxia Affects Pulmonary Artery Contractile Functions via Downregulating L-type CaJournal of the American Heart Association · 2021Article
- MARCKS mediates vascular contractility through regulating interactions between voltage-gated CaVascular pharmacology · 2020Article
- Prenatal hypoxia inhibited propionate-evoked BK channels of mesenteric artery smooth muscle cells in offspring.Journal of cellular and molecular medicine · 2020Article
- Prenatal metyrapone treatment modulates neonatal cerebrovascular structure, function, and vulnerability to mild hypoxic-ischemic injury.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Prenatal hypoxia affected endothelium-dependent vasodilation in mesenteric arteries of aged offspring via increased oxidative stress.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
- Inherited risk plus prenatal insult caused malignant dysfunction in mesenteric arteries in adolescent SHR offspring.PloS one · 2019Article
- Magnesium Sulfate-Mediated Vascular Relaxation and Calcium Channel Activity in Placental Vessels Different From Nonplacental Vessels.Journal of the American Heart Association · 2018Article
- Prenatal Hypoxia Induced Dysfunction in Cerebral Arteries of Offspring Rats.Journal of the American Heart Association · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypoxia during pregnancy could cause abnormal development and lead to increased risks of vascular diseases in adults. This study determined angiotensin II (AII)-mediated vascular dysfunction in offspring middle cerebral arteries (MCA). METHODS AND
resultsPregnant rats were subjected to hypoxia. Vascular tension in offspring MCA by AII with or without inhibitors, calcium channel activities, and endoplasmic reticulum calcium stores were tested. Whole-cell patch clamping was used to investigate voltage-dependent calcium channel currents. mRNA expression was tested using quantitative real-time polymerase chain reaction. AII-mediated MCA constriction was greater in male offspring exposed to prenatal hypoxia. AT1 and AT2 receptors were involved in the altered AII-mediated vasoconstriction. Prenatal hypoxia increased baseline activities of L-type calcium channel currents in MCA smooth muscle cells. However, calcium currents stimulated by AII were not significantly changed, whereas nifedipine inhibited AII-mediated vasoconstrictions in the MCA. Activities of IP
conclusionsHypoxia in pregnancy could induce dysfunction in both contraction and dilation in the offspring MCA. AII-increased constriction in the prenatal-hypoxia group was not mainly dependent on the L-type and T-type calcium channels; it might predominantly rely on the AII receptors, IP
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