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首页> 外文期刊>American Journal of Physiology >Aquaporin-1 facilitates pressure-driven water flow across the aortic endothelium
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Aquaporin-1 facilitates pressure-driven water flow across the aortic endothelium

机译：Aquaporin-1促进压力驱动的水流过主动脉内皮

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摘要

Aquaporin-1, a ubiquitous water channel membrane protein, is a major contributor to cell membrane osmotic water permeability. Arteries are the physiological system where hydrostatic dominates osmotic pressure differences. In the present study, we show that the walls of large conduit arteries constitute the first example where hydrostatic pressure drives aquaporin-1-mediated transcellular/transendothelial flow. We studied cultured aortic endothelial cell monolayers and excised whole aortas of male Sprague-Dawley rats with intact and inhibited aquaporin-1 activity and with normal and knocked down aquaporin-1 expression. We subjected these systems to transmural hydrostatic pressure differences at zero osmotic pressure differences. Impaired aquaporin-1 endothelia consistently showed reduced engineering flow metrics (transendothelial water flux and hydraulic conductivity). In vitro experiments with tracers that only cross the endothelium paracellularly showed that changes in junc-tional transport cannot explain these reductions. Percent reductions in whole aortic wall hydraulic conductivity with either chemical blocking or knockdown of aquaporin-1 differed at low and high transmural pressures. This observation highlights how aquaporin-1 expression likely directly influences aortic wall mechanics by changing the critical transmural pressure at which its sparse subendothelial intima compresses. Such compression increases transwall flow resistance. Our endothelial and historic erythrocyte membrane aquaporin density estimates were consistent. In conclusion, aquaporin-1 significantly contributes to hydrostatic pressure-driven water transport across aortic endothelial monolayers, both in culture and in whole rat aortas. This transport, and parallel junctional flow, can dilute solutes that entered the wall paracellularly or through endothelial monolayer disruptions. Lower atherogenic precursor solute concentrations may slow their intimal entrainment kinetics.
机译：Aquaporin-1，一种无处不在的水通道膜蛋白，是细胞膜渗透渗透性的主要因素。动脉是静液栓渗透渗透压差异的生理系统。在本研究中，我们表明大导管动脉的壁构成了静水压力驱动Aquaporin-1介导的型造型术/横向流程的第一示例。我们研究了培养的主动脉内皮细胞单层，并在完整和抑制水上素-1活性并抑制水上蛋白-1活性并敲下水上蛋白-1表达的整个主动脉。我们使这些系统在零渗透压差异以透过液压压力差异。 Apirated Aquaporin-1内皮且始终显示出降低的工程流量度量（Transendithelial水通量和液压导电）。体外实验与梯子仅横跨阴道内皮，表明junc型运输的变化无法解释这些减少。整个主动脉壁液压导电率的百分比减少，化学阻挡或水坑蛋白-1的敲低在低透气压力下不同。该观察结果突出了Aquaporin-1表达式如何通过改变其稀疏下属内膜内膜压缩的临界透气压力来影响主动脉壁机械。这种压缩增加了横磨机的流动阻力。我们的内皮和历史性红细胞膜水上素密度估计是一致的。总之，Aquaporin-1在培养和全大鼠主动脉中横跨主动脉内皮单层的静压压力驱动水输送。这种运输和平行的连接流动可以稀释，溶质，使壁上或通过内皮单层破坏进入壁。较低的肌动蛋白前体溶质浓度可能会减缓其内衣夹带动力学。

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