Regulatory roles of nitric oxide and angiotensin II on renal tubular transport.
Regulatory roles of nitric oxide and angiotensin II on renal tubular transport.
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DOI：
10.5527/wjn.v3.i4.295
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发表时间：
2014-11
期刊：
影响因子：
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通讯作者：
S. Horita;M. Nakamura;Ayumi Shirai;O. Yamazaki;N. Satoh;Masashi Suzuki;G. Seki
中科院分区：
文献类型：
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作者：
S. Horita;M. Nakamura;Ayumi Shirai;O. Yamazaki;N. Satoh;Masashi Suzuki;G. Seki
肾小管调节血压和体液动态平衡。在调节溶质和水的运输方面发挥重要作用的介质包括血管紧张素II(AngII)和一氧化氮(NO)。血管紧张素转换酶II可通过对心脏、血管系统和肾小管的影响而显著升高血压。血管紧张素转换酶一般通过触发钠和液体滞留在几乎所有的肾小管段来刺激钠的重吸收。肾近端小管(PT)转运的刺激被认为是血管紧张素Ⅱ介导的高血压的关键。然而，血管紧张素转换酶在小鼠、大鼠和兔体内的体外转运有两个阶段的作用：低浓度刺激和高浓度抑制。另一方面，NO通常被认为抑制肾小管运输。在PTS中，NO似乎参与了血管紧张素Ⅱ的抑制作用。最近的一项研究报告了一个令人惊讶的发现：血管紧张素转换酶对人体PT运输具有单相刺激作用。对信号机制的详细分析表明，与其他物种不同，人的NO/3‘，5’-环鸟苷/细胞外信号调节激酶通路似乎介导了Ang II对PT转运的这种作用。在这篇综述中，我们将讨论最近的进展，了解血管紧张素转换酶和一氧化氮对肾小管转运的影响。
Renal tubules regulate blood pressure and humoral homeostasis. Mediators that play a significant role in regulating the transport of solutes and water include angiotensin II (AngII) and nitric oxide (NO). AngIIcan significantly raise blood pressure via effects on the heart, vasculature, and renal tubules. AngII generally stimulates sodium reabsorption by triggering sodium and fluid retention in almost all segments of renal tubules. Stimulation of renal proximal tubule (PT) transport is thought to be essential for AngII-mediated hypertension. However, AngII has a biphasic effect on in vitro PT transport in mice, rats, and rabbits: stimulation at low concentrations and inhibition at high concentrations. On the other hand, NO is generally thought to inhibit renal tubular transport. In PTs, NO seems to be involved in the inhibitory effect of AngII. A recent study reports a surprising finding: AngII has a monophasic stimulatory effect on human PT transport. Detailed analysis of signalling mechanisms indicates that in contrast to other species, the human NO/guanosine 3',5'-cyclic monophosphate/extracellular signal-regulated kinase pathway seems to mediate this effect of Ang II on PT transport. In this review we will discuss recent progress in understanding the effects of AngII and NO on renal tubular transport.