ArticleHypertension research : official journal of the Japanese Society of Hypertension2022
In utero hypoxia attenuated acetylcholine-mediated vasodilatation via CHRM3/p-NOS3 in fetal sheep MCA: role of ROS/ERK1/2.
Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 4 citations in OpenAlex.
- Muscarinic acetylcholine receptor 3 localized to primary endothelial cilia regulates blood pressure and cognition.Scientific reports · 2025Article
- Gestational Hypoxia Impaired Endothelial Nitric Oxide Synthesis Via miR-155-5p/NADPH Oxidase/Reactive Oxygen Species Axis in Male Offspring Vessels.Journal of the American Heart Association · 2024Article
- Associations of genetic variations in the M3 receptor with salt sensitivity, longitudinal changes in blood pressure and the incidence of hypertension in Chinese adults.Journal of clinical hypertension (Greenwich, Conn.) · 2024Article
- The Brain at High Altitude: From Molecular Signaling to Cognitive Performance.International journal of molecular sciences · 2023Review
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10 authors at 2 institutions in 1 country.
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Abstract
Hypoxia can lead to adult middle cerebral artery (MCA) dysfunction and increase the risk of cerebrovascular diseases. It is largely unknown whether intrauterine hypoxia affects fetal MCA vasodilatation. This study investigated the effects and mechanisms of intrauterine hypoxia on fetal MCA vasodilatation. Near-term fetal sheep were exposed to intrauterine hypoxia. Human umbilical vein endothelial cells (HUVECs) were exposed to hypoxia in cellular experiments. Vascular tone measurement, molecular analysis, and transmission electron microscope (TEM) were utilized to determine vascular functions, tissue anatomy, and molecular pathways in fetal MCA. In fetal MCA, acetylcholine (ACh) induced reliable relaxation, which was markedly attenuated by intrauterine hypoxia. Atropine, P-F-HHSiD, L-NAME, and u0126 blocked most ACh-mediated dilation, while AF-DX 116 and tropicamide partially inhibited the dilation. Indomethacin and SB203580 did not significantly change ACh-mediated dilation. Tempol and PS-341 could restore the attenuated ACh-mediated vasodilatation following intrauterine hypoxia. The mRNA expression levels of CHRM2 and CHRM3 and the protein levels of CHRM3, p-NOS3, SOD2, ERK1/2, p-ERK1/2, MAPK14, and p-MAPK14 were significantly reduced by intrauterine hypoxia. The dihydroethidium assay showed that the production of ROS was increased under intrauterine hypoxia. TEM analysis revealed endothelial cells damaged by intrauterine hypoxia. In HUVECs, hypoxia increased ROS formation and decreased the expression of CHRM3, p-NOS3, SOD1, SOD2, SOD3, ERK1/2, p-ERK1/2, and p-MAPK14, while tempol and PS-341 potentiated p-NOS3 protein expression. In conclusion, in utero hypoxia reduced ACh-mediated vasodilatation in ovine MCA predominantly via decreased CHRM3 and p-NOS3, and the decreased NOS3 bioactivities might be attributed to ROS and ERK1/2.
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