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Authors:Zhao Meng; Li Huan; Ji Bingyu; Xu Ting; Gao Qinqin
Keywords:prenatal hypoxia;pulmonary artery;vasoconstriction;vasodilation;calcium channels
DOI:10.19405/j.cnki.issn1000-1492.2022.02.014
〔Abstract〕 Objective To investigate the effect and mechanism of prenatal hypoxia on pulmonary artery vascular function in adult male offspring. Methods Sprague-Dawley pregnant rats were randomly divided into hypoxia group and control group. Pregnant rats in the hypoxia group were housed in the hypoxia chamber(a mixture of 89.5% nitrogen gas and 10.5% oxygen) from gestational day 10 th to 20 th. Pregnant rats in the control group were fed under normal oxygen. All animals were fed with standard rat food and tap water, and allowed to give birth naturally. After weaning, the male offspring were raised to 4 months old. Male offspring rats were anesthetized with chloral hydrate, and pulmonary artery was isolated for vascular function and molecular experiments. Results Compared with the control group, phenylephrine(PE)-induced contraction response in prenatal hypoxic pulmonary artery was decreased(P<0.001). There was no difference in acetyl choline(ACH)-and sodium nitrate(SNP)-induced diastolic responses between the two groups. Compared with control group, Cav1.2 protein(P<0.01) and mRNA levels(P<0.001) in hypoxia group were reduced. Conclusion Prenatal hypoxia can lead to a decreased PE-induced vasoconstriction response in adult male offspring, which is related to the down-regulation of Cav1.2 expression in pulmonary artery.