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首页> 外文期刊>American Journal of Physiology >Impaired NO signaling in small pulmonary arteries of chronically hypoxic newborn piglets.
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Impaired NO signaling in small pulmonary arteries of chronically hypoxic newborn piglets.

机译：慢性缺氧新生仔猪小肺动脉中NO信号受损。

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摘要

We performed studies to determine whether chronic hypoxia impairs nitric oxide (NO) signaling in resistance level pulmonary arteries (PAs) of newborn piglets. Piglets were maintained in room air (control) or hypoxia (11% O(2)) for either 3 (shorter exposure) or 10 (longer exposure) days. Responses of PAs to a nonselective NO synthase (NOS) antagonist, N(omega)-nitro-L-arginine methylester (L-NAME), a NOS-2-selective antagonist, aminoguanidine, and 7-nitroindazole, a NOS-1-selective antagonist, were measured. Levels of NOS isoforms and of two proteins involved in NOS signaling, heat shock protein (HSP) 90 and caveolin-1, were assessed in PA homogenates. PAs from all groups constricted to L-NAME but not to aminoguanidine or 7-nitroindazole. The magnitude of constriction to L-NAME was similar for PAs from control and hypoxic piglets of the shorter exposure period but was diminished for PAs from hypoxic compared with control piglets of the longer exposure period. NOS-3, HSP90, and caveolin-1 levels were similar in hypoxic and control PAs. These findings indicate that NOS-3, but not-NOS 2 or NOS-1, is involved with basal NO production in PAs from both control and hypoxic piglets. After 10 days of hypoxia, NO function is impaired in PAs despite preserved levels of NOS-3, HSP90, and caveolin-1. The development of NOS-3 dysfunction in resistance level PAs may contribute to the progression of chronic hypoxia-induced pulmonary hypertension in newborn piglets.
机译：我们进行了研究以确定慢性缺氧是否会损害新生仔猪抗性水平的肺动脉（PA）中的一氧化氮（NO）信号。将仔猪保持在室内空气（对照）或缺氧（11％O（2））中3天（较短的暴露时间）或10天（较长的暴露时间）。 PA对非选择性NO合酶（NOS）拮抗剂，N（ω）-硝基-L-精氨酸甲酯（L-NAME），NOS-2选择性拮抗剂，氨基胍和7-硝基吲唑（NOS-1-）的反应测量选择性拮抗剂。在PA匀浆中评估了NOS亚型和参与NOS信号传导的两种蛋白质的水平，即热激蛋白（HSP）90和小窝蛋白1。所有组的PA仅局限于L-NAME，但不限于氨基胍或7-硝基吲唑。暴露时间较短的对照仔猪和低氧仔猪对PA的L-NAME收缩幅度相似，但暴露时间较长的对照仔猪与低氧仔猪的PA对L-NAME的收缩程度却有所降低。低氧和对照PA中的NOS-3，HSP90和Caveolin-1水平相似。这些发现表明，NOS-3（而非NOS 2或NOS-1）与对照仔猪和低氧仔猪的PA中的基础NO产生有关。缺氧10天后，尽管NOS-3，HSP90和Caveolin-1的水平保持不变，但PA中的NO功能受损。耐药水平PAs中NOS-3功能障碍的发展可能有助于新生仔猪慢性低氧引起的肺动脉高压的发展。

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