Oxidative consumption of nitric oxide: a potential mediator of uremic vascular disease.
Oxidative consumption of nitric oxide: a potential mediator of uremic vascular disease.
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一氧化氮的氧化消耗：尿毒症血管疾病的潜在介质。
DOI：
10.1046/j.1523-1755.63.s84.41.x
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Muhammad M. Yaqoob
中科院分区：
文献类型：
--
作者：
Raj Thuraisingham;Muhammad M. Yaqoob
最近的数据引起了我们对尿毒症患者血管生物力学特性改变与左心室肥厚（LVH）之间关系的关注。我们已经能够证明尿毒症导致大鼠导管血管的功能改变，在结构改变之前，独立于血压。由于一氧化氮（NO）是一种有效的心血管系统调节剂，我们研究了NO在尿毒症中的途径。现有的数据有些令人困惑，一些人认为一氧化氮系统是上调的，而另一些人则相反。然而，当仔细检查时，出现了一种模式，检查NO释放的研究显示产量增加，而检查NO生物活性的研究显示其减弱。我们假设在尿毒症中一氧化氮释放增加，但过量消耗。我们自己的关于健康年轻男性血液透析患者血清中NO代谢物（NOx）的数据表明，与对照组相比，透析前和透析后的浓度都更高。由于内皮是一氧化氮的潜在来源，我们在尿毒症血浆中培养内皮细胞。这些研究表明，与对照组相比，在尿毒症条件下培养的细胞增加了基础NO释放。此外，精氨酸代谢的改变似乎发挥了作用，因为有证据表明这些细胞中的精氨酸酶活性降低，从而增加了NO途径的精氨酸可用性。鉴于尿毒症综合征的体内数据和临床特征表明一氧化氮生物活性降低，我们研究了过量产生的一氧化氮被消耗并变得无生物活性的可能性。尿毒症大鼠和对照大鼠的主动脉染色检测硝基酪氨酸的存在。所有尿毒症主动脉均呈阳性，但对照主动脉未检测到硝基酪氨酸。
Recent data has drawn our attention to the relationship between altered biomechanical properties of the vasculature and left ventricular hypertrophy (LVH) in uremia. We have been able to show that uremia causes functional changes in the conduit vessels of rats, predating structural changes and independent of blood pressure. As nitric oxide (NO) is a potent modulator of the cardiovascular system, we studied the NO pathway in uremia. The existing data are somewhat confusing, with some suggesting up-regulation of the NO system, and others the opposite. When examined critically, however, a pattern emerges, with studies examining NO release showing increased production, whereas those examining NO bioactivity show it to be attenuated. We hypothesized that there is increased NO release, but excess consumption in uremia. Our own data on NO metabolites (NOx) in the serum of healthy young male hemodialysis patients indicate higher concentrations both pre- and post-dialysis compared to controls. As the endothelium is a potential source of NO, we cultured endothelial cells in uremic plasma. These studies demonstrated increased basal NO release from cells cultured under uremic conditions compared to controls. Furthermore, alterations in arginine metabolism appear to play a role, as there is evidence for reduced arginase activity in these cells, thereby increasing arginine availability for the NO pathway. Given the in vivo data and clinical characteristics of the uremic syndrome suggesting reduced NO bioactivity, we examined the possibility that the excess NO generated is being consumed and rendered bio-inactive. Aortae from uremic and control rats were stained for the presence of nitrotyrosine. All uremic aortae stained positively, but nitrotyrosine was not present in any control aortae.
DOI：
10.1016/s0272-6386(99)70348-3
发表时间：
1999-08
期刊：
American journal of kidney diseases : the official journal of the National Kidney Foundation
影响因子：
--
作者：
Rebecca J. Schmidt;Jennifer Domico;L. Samsell;Stanley Yokota;Timothy S. Tracy;Michael I. Sorkin;K. Engels;C. Baylis
通讯作者：
Rebecca J. Schmidt;Jennifer Domico;L. Samsell;Stanley Yokota;Timothy S. Tracy;Michael I. Sorkin;K. Engels;C. Baylis
影响因子：
19.6
作者：
Schmidt, RJ;Baylis, C
通讯作者：
Baylis, C
肾衰竭增加大鼠胃粘膜血流量和酸分泌：内皮源性一氧化氮的作用。
DOI：
10.1152/ajpgi.1992.263.1.g75
发表时间：
1992
期刊：
The American journal of physiology
影响因子：
--
作者：
Quintero,E;Guth,PH
通讯作者：
Guth,PH