Zhang Wensheng, Edwards Aurélie
Department of Chemical and Biological Engineering, Tufts University, 4 Colby St., Medford, MA 02155, USA.
Am J Physiol Renal Physiol. 2003 Oct;285(4):F731-47. doi: 10.1152/ajprenal.00172.2003. Epub 2003 Jun 24.
A mathematical model of transport in the renal medullary microcirculation was used to investigate the role of the UTB urea transporter expressed in descending vasa recta (DVR) endothelia and red blood cell (RBC) membranes. Our simulations suggest that UTB raises RBC and plasma and interstitial urea concentrations by facilitating radial diffusion of the solute and therefore serves to increase the contribution of urea to the corticomedullary osmolality gradient, assuming no secondary effects on tubular transport. However, by lowering transmural urea concentration gradients, UTB reduces water efflux from DVR through aquaporin-1 (AQP1) water channels, thereby decreasing plasma sodium concentration. The net result of these competing effects on the osmolality gradient depends on the fraction of filtered urea that is reabsorbed by vasa recta. We also found that the contribution of UTB to water transport across DVR and RBCs is negligible, even in the absence of AQP1. Our model predicts that UTB plays a significant role, however, in reducing the shrinking and swelling of RBCs as blood flows along the medulla.
利用肾髓质微循环中的转运数学模型,研究了降支直小血管(DVR)内皮和红细胞(RBC)膜中表达的UTB尿素转运体的作用。我们的模拟结果表明,假设对肾小管转运没有继发影响,UTB通过促进溶质的径向扩散提高红细胞、血浆和间质尿素浓度,因此有助于增加尿素对皮质髓质渗透压梯度的贡献。然而,通过降低跨膜尿素浓度梯度,UTB减少了通过水通道蛋白-1(AQP1)水通道从DVR流出的水量,从而降低了血浆钠浓度。这些对渗透压梯度的竞争效应的净结果取决于直小血管重吸收的滤过尿素分数。我们还发现,即使在没有AQP1的情况下,UTB对水通过DVR和RBC的转运贡献也可以忽略不计。然而,我们的模型预测,随着血液沿髓质流动,UTB在减少RBC的收缩和肿胀方面起着重要作用。