后代
肠系膜动脉
内分泌学
内科学
伊诺斯
一氧化氮
硝普钠
血管舒张
苯肾上腺素
环磷酸鸟苷
内皮
血管平滑肌
一氧化氮合酶
医学
化学
生物
血压
动脉
怀孕
遗传学
平滑肌
作者
Xinquan Wang,Jialiang Wang,Hao Luo,Caiyu Chen,Fang Pei,Yuchen Cai,Xiaoli Yang,Na Wang,Jinjuan Fu,Zaichen Xu,Lin Zhou,Chunyu Zeng
标识
DOI:10.1016/j.freeradbiomed.2015.05.040
摘要
Cardiovascular diseases, such as hypertension, could be programmed in fetal life. Prenatal lipopolysaccharide (LPS) exposure in utero results in increased blood pressure in offspring, but the vascular mechanisms involved are unclear. Pregnant Sprague-Dawley rats were intraperitoneally injected with LPS (0.79mg/kg) or saline (0.5ml) on gestation days 8, 10, and 12. The offspring of LPS-treated dams had higher blood pressure and decreased acetylcholine (ACh)-induced relaxation and increased phenylephrine (PE)-induced contraction in endothelium-intact mesenteric arteries. Endothelium removal significantly enhanced the PE-induced contraction in offspring of control but not LPS-treated dams. The arteries pretreated with l-NAME to inhibit nitric oxide synthase (eNOS) in the endothelium or ODQ to inhibit cGMP production in the vascular smooth muscle had attenuated ACh-induced relaxation but augmented PE-induced contraction to a larger extent in arteries from offspring of control than those from LPS-treated dams. In addition, the endothelium-independent relaxation caused by sodium nitroprusside was also decreased in arteries from offspring of LPS-treated dams. The functional results were accompanied by a reduction in the expressions of eNOS and soluble guanylate cyclase (sGC) and production of NO and cGMP in arteries from offspring of LPS-treated dams. Furthermore, LPS-treated dam's offspring arteries had increased oxidative stress and decreased antioxidant capacity. Three-week treatment with TEMPOL, a reactive oxygen species (ROS) scavenger, normalized the alterations in the levels of ROS, eNOS, and sGC, as well as in the production of NO and cGMP and vascular function in the arteries of the offspring of LPS-treated dams. In conclusion, prenatal LPS exposure programs vascular dysfunction of mesenteric arteries through increased oxidative stress and impaired NO-cGMP signaling pathway.
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