Department of Medical Cell Biology, University of Uppsala, Uppsala, Sweden.
Institute of Vegetative Physiology, Charite-Universitätsmedizin Berlin, Berlin, Germany.
Acta Physiol (Oxf). 2018 Feb;222(2). doi: 10.1111/apha.12925. Epub 2017 Aug 19.
Afferent arterioles (AA) hold a key position in the regulation of renal blood flow and glomerular filtration rate. Being the effector site of tubuloglomerular feedback, the afferent arteriole contributes to the renal handling of sodium and fluid. Dehydration goes along with increased renal interstitial protein concentration. Here, the hypothesis was tested that extravasal protein concentration directly modulates afferent arteriolar tone, a mechanism which may contribute to body fluid volume control.
The effect of increased extravasal albumin concentration on the vascular reactivity was investigated in renal AA and interlobar arteries of mice, in rat renal AA and in pancreatic islet arterioles.
Albumin (2 and 4% in the bath solution) significantly potentiated the contractile response of renal afferent arterioles induced by angiotensin II and adenosine, as well as their combination, compared to the control situation (0.1% albumin). Albumin did not influence the contractility of larger renal vessels or pancreatic islet arterioles. Mimicking the increase in the osmolality induced by 4% albumin by applying mannitol to the bath solution also increased the response of renal arterioles to Ang II. However, the effect was smaller compared to that of albumin. The nitric oxide bioavailability, measured by DAF-FM fluorescence, was reduced in afferent arterioles exposed to 4% albumin.
The protein-induced modulation of AA tone is mediated by the increased osmolality as well as by NO scavenging. The results suggest a possible contribution of these mechanisms to the control of extracellular fluid volume via adjustment of renal blood flow and glomerular filtration rate.
入球小动脉（AA）在调节肾血流量和肾小球滤过率方面起着关键作用。作为管球反馈的效应部位，入球小动脉有助于肾脏对钠和液体的处理。脱水伴随着肾间质蛋白浓度的增加。在这里，我们假设额外的血管外蛋白浓度直接调节入球小动脉的张力，这一机制可能有助于控制体液量。
研究了增加的血管外白蛋白浓度对小鼠肾入球小动脉和小叶间动脉、大鼠肾入球小动脉和胰岛动脉血管反应性的影响。
与对照情况（0.1%白蛋白）相比，白蛋白（浴液中 2%和 4%）显著增强了血管紧张素 II 和腺苷诱导的肾入球小动脉的收缩反应，以及它们的组合。白蛋白不影响较大的肾血管或胰岛动脉的收缩性。通过将甘露醇应用于浴液来模拟 4%白蛋白引起的渗透压增加，也增加了肾动脉对 Ang II 的反应。然而，与白蛋白相比，效果较小。在暴露于 4%白蛋白的入球小动脉中，测量到的一氧化氮生物利用度（通过 DAF-FM 荧光）降低。
AA 张力的蛋白诱导调节是由渗透压增加以及 NO 清除介导的。这些结果表明，这些机制可能通过调节肾血流量和肾小球滤过率来参与细胞外液体积的控制。
