Strieter J, Weinstein A M, Giebisch G, Stephenson J L
Department of Physiology and Biophysics, Cornell University Medical College, New York, New York 10021.
Am J Physiol. 1992 Dec;263(6 Pt 2):F1076-86. doi: 10.1152/ajprenal.1992.263.6.F1076.
The effect of luminal flow rate and peritubular pH on Na and K transport is investigated in a mathematical model of the rabbit cortical collecting tubule. The model is used to simulate a 0.4-cm segment of tubule comprised of principal cell, alpha- and beta-intercalated cells, and lateral interspace. Calculations produce luminal profiles of Na, K, Cl, HCO3, and phosphate, as well as of electrical potential and pH. Parameter sets are developed that permit representation of both unstimulated and deoxycorticosterone acetate-stimulated tubules. A series of simulations is performed in which initial luminal flow rate is varied over the range of values between 0.1 and 30 nl/min. A marked flow-dependent enhancement of Na reabsorption and K secretion is seen, especially at lower flows, while Cl and HCO3 transport remain relatively constant. In experimental studies, it has been observed that metabolic alkalosis stimulates and metabolic acidosis inhibits K secretion, while leaving Na transport relatively unaffected [B. A. Stanton and G. Giebisch. Am. J. Physiol. 242 (Renal Fluid Electrolyte Physiol. 11): F544-F551, 1982; K. Tabei, S. Muto, Y. Ando, Y. Sakairi, and Y. Asano. J. Am. Soc. Nephrol. 1: 693, 1990; and K. Tabei, S. Muto, H. Furuya, and Y. Asano. J. Am. Soc. Nephrol. 2: 752, 1991]. Model calculations indicate that, when ion permeabilities are fixed and not dependent on pH, the impact of peritubular HCO3 on K secretion cannot be simulated. When junctional Cl permeability decreases with increasing interspace pH (E. M. Wright and J. M. Diamond. Biochim. Biophys. Acta 163: 57-74, 1968) in the model, there is a marked stimulation of K secretion with alkalosis and inhibition with acidosis. Furthermore, inclusion of a pH-dependent apical Na permeability [L. G. Palmer and G. Frindt. Am. J. Physiol. 253 (Renal Fluid Electrolyte Physiol. 22): F333-F339, 1987] that increases with increasing principal cell pH significantly reduces the change in Na+ reabsorption seen with the pH-dependent junctional Cl permeability alone. In these calculations, a pH-dependent apical K permeability [W. Wang, A. Schwab, and G. Giebisch. Am. J. Physiol. 259 (Renal Fluid Electrolyte Physiol. 28): F494-F502, 1990] that increases with increasing principal cell pH shows relatively little impact on K secretion.
在兔皮质集合管的数学模型中，研究了管腔流速和肾小管周pH值对钠和钾转运的影响。该模型用于模拟由主细胞、α和β闰细胞以及侧间隙组成的0.4厘米长的肾小管节段。计算得出钠、钾、氯、碳酸氢根和磷酸盐的管腔分布，以及电势和pH值。开发了参数集，可用于表示未受刺激和醋酸脱氧皮质酮刺激的肾小管。进行了一系列模拟，其中初始管腔流速在0.1至30 nl/分钟之间变化。观察到钠重吸收和钾分泌明显依赖于流速增强，尤其是在较低流速时，而氯和碳酸氢根的转运保持相对恒定。在实验研究中，已观察到代谢性碱中毒刺激而代谢性酸中毒抑制钾分泌，而钠转运相对不受影响[B.A.斯坦顿和G.吉比施。《美国生理学杂志》242(肾脏液体电解质生理学11):F544 - F551，1982；K.田部、S.武藤、Y.安藤、Y.坂井和Y.浅野。《美国肾脏病学会杂志》1:693，1990；以及K.田部、S.武藤、H.古屋和Y.浅野。《美国肾脏病学会杂志》2:752，1991]。模型计算表明，如果离子通透性固定且不依赖于pH值，则无法模拟肾小管周碳酸氢根对钾分泌的影响。当模型中连接部氯通透性随间隙pH值升高而降低时(E.M.赖特和J.M.戴蒙德。《生物化学与生物物理学报》(生物化学与生物物理学报)163:57 - 74，1968)，碱中毒时钾分泌明显受刺激，酸中毒时则受抑制。此外，纳入随主细胞pH值升高而增加的pH依赖性顶端钠通透性[L.G.帕尔默和G.弗林特。《美国生理学杂志》253(肾脏液体电解质生理学22):F333 - F339，1987]，可显著降低仅由pH依赖性连接部氯通透性引起的钠重吸收变化。在这些计算中，随主细胞pH值升高而增加的pH依赖性顶端钾通透性[W.王、A.施瓦布和G.吉比施。《美国生理学杂志》259(肾脏液体电解质生理学28):F494 - F502，1990]对钾分泌的影响相对较小。
