Interactions between arterial pressure and sodium excretion.
Interactions between arterial pressure and sodium excretion.
复制标题
动脉压和钠排泄之间的相互作用。
DOI：
10.1097/00041552-199601000-00012
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发表时间：
1996
影响因子：
3.2
通讯作者：
Majid,DS
中科院分区：
文献类型：
--
作者：
Navar,LG;Majid,DS
最近的发展导致了对介导钠排泄响应于动脉压变化的变化的机制的重新关注，这种现象称为压力尿钠排泄。压力性尿钠排泄发生在滤过负荷没有变化的情况下，因此钠排泄的变化是由肾小管钠重吸收的变化引起的。近端和远端肾单位节段都被认为是重吸收改变的部位。压力性尿钠排泄的具体机制尚未解决。一种建议认为，肾间质液压力的变化可能部分是由于肾髓质循环的自动调节效率低于皮质，改变了钠的重吸收。另外，最近的研究表明，动脉压的增加增加了内皮一氧化氮的形成，这通过对肾小管的直接作用以及血液动力学介导的作用来抑制钠重吸收。
Recent developments have led to renewed interest in the mechanisms that mediate the changes in sodium excretion in response to changes in arterial pressure, a phenomenon termed pressure-natriuresis. Pressure-natriuresis occurs in the absence of changes in filtered load and thus, the changes in sodium excretion are caused by changes in net tubular sodium reabsorption. Both proximal and distal nephron segments have been implicated as the sites of altered reabsorption. The specific mechanism responsible for pressure-natriuresis remains unresolved. One proposal suggests that changes in renal interstitial fluid pressure which may be due, in part, to a less efficient autoregulation of the renal medullary circulation than of the cortex, alter sodium reabsorption. Alternatively, recent studies indicate that increases in arterial pressure increase endothelial nitric oxide formation which inhibits sodium reabsorption via direct effects on the tubules as well as hemodynamically mediated effects.