Edwards Aurélie, Layton Anita T
Department of Biomedical Engineering, Boston University, Boston, MA, 02215, USA.
Departments of Mathematics and Biomedical Engineering, Duke University, Durham, NC, 27708-0320, USA.
Bull Math Biol. 2017 Nov;79(11):2512-2533. doi: 10.1007/s11538-017-0338-6. Epub 2017 Sep 12.
We developed a dynamic model of a rat proximal convoluted tubule cell in order to investigate cell volume regulation mechanisms in this nephron segment. We examined whether regulatory volume decrease (RVD), which follows exposure to a hyposmotic peritubular solution, can be achieved solely via stimulation of basolateral K[Formula: see text] and [Formula: see text] channels and [Formula: see text]-[Formula: see text] cotransporters. We also determined whether regulatory volume increase (RVI), which follows exposure to a hyperosmotic peritubular solution under certain conditions, may be accomplished by activating basolateral [Formula: see text]/H[Formula: see text] exchangers. Model predictions were in good agreement with experimental observations in mouse proximal tubule cells assuming that a 10% increase in cell volume induces a fourfold increase in the expression of basolateral K[Formula: see text] and [Formula: see text] channels and [Formula: see text]-[Formula: see text] cotransporters. Our results also suggest that in response to a hyposmotic challenge and subsequent cell swelling, [Formula: see text]-[Formula: see text] cotransporters are more efficient than basolateral K[Formula: see text] and [Formula: see text] channels at lowering intracellular osmolality and reducing cell volume. Moreover, both RVD and RVI are predicted to stabilize net transcellular [Formula: see text] reabsorption, that is, to limit the net [Formula: see text] flux decrease during a hyposmotic challenge or the net [Formula: see text] flux increase during a hyperosmotic challenge.
我们构建了大鼠近端肾小管细胞的动态模型,以研究该肾单位节段中的细胞体积调节机制。我们研究了暴露于低渗性肾小管周围溶液后发生的调节性容积减小(RVD)是否仅通过刺激基底外侧K⁺和Cl⁻通道以及Na⁺-K⁺-2Cl⁻协同转运体就能实现。我们还确定了在某些条件下暴露于高渗性肾小管周围溶液后发生的调节性容积增加(RVI)是否可通过激活基底外侧Na⁺/H⁺交换体来实现。假设细胞体积增加10%会导致基底外侧K⁺和Cl⁻通道以及Na⁺-K⁺-2Cl⁻协同转运体的表达增加四倍,模型预测结果与小鼠近端小管细胞的实验观察结果高度一致。我们的结果还表明,在应对低渗性刺激和随后的细胞肿胀时,Na⁺-K⁺-2Cl⁻协同转运体在降低细胞内渗透压和减小细胞体积方面比基底外侧K⁺和Cl⁻通道更有效。此外,预计RVD和RVI均可稳定跨细胞Na⁺重吸收净值,即在低渗性刺激期间限制Na⁺通量净减少,或在高渗性刺激期间限制Na⁺通量净增加。