Clinical Pharmacology Research Unit, Division of Clinical Pharmacology, Department of Medicine, Miller School of Medicine, University of Miami, Miami, Florida 33136, USA.
Kidney Int. 2012 Dec;82(12):1313-20. doi: 10.1038/ki.2012.269. Epub 2012 Aug 8.
A gastrointestinal-renal natriuretic signaling axis has been proposed to regulate sodium excretion in response to acute sodium ingestion. Such an axis is thought to be regulated by a gastrointestinal sodium sensor coupled to the activation/release of a natriuretic signal and could have important clinical and scientific implications. Here we systematically tested for this putative axis and the potential involvement of the gastrointestinal-derived natriuretic prohormones prouroguanylin and proguanylin in 15 healthy volunteers. There was no difference in sodium excretion following equivalent oral or intravenous sodium loads during either high- or low-sodium diets. Furthermore, serum concentrations of prouroguanylin and proguanylin did not increase, did not differ following oral or intravenous sodium, and did not correlate with sodium excretion. Thus, our results do not support an acute gastrointestinal-renal natriuretic axis or a central role for prouroguanylin or proguanylin in humans. If such an axis does exist, it is not characterized by a significant difference in the pattern of sodium excretion following either an oral or intravenous sodium load.
已经提出了一个胃肠肾利钠信号轴，以响应急性钠摄入来调节钠排泄。这种轴被认为是由与利钠信号的激活/释放偶联的胃肠钠传感器调节的，可能具有重要的临床和科学意义。在这里，我们系统地测试了这种假定的轴以及胃肠衍生的利钠前体尿鸟苷素和胍鸟苷素在 15 名健康志愿者中的潜在作用。在高钠或低钠饮食期间，口服或静脉给予等量的钠负荷后，钠排泄没有差异。此外，尿鸟苷素和胍鸟苷素的血清浓度没有增加，口服或静脉给予钠后没有差异，也与钠排泄无关。因此，我们的结果不支持急性胃肠肾利钠轴或尿鸟苷素或胍鸟苷素在人体中的核心作用。如果存在这样的轴，那么无论是口服还是静脉给予钠负荷后，钠排泄的模式都没有显著差异。
