Sun A, Grossman E B, Lombardi M, Hebert S C
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.
J Membr Biol. 1991 Feb;120(1):83-94. doi: 10.1007/BF01868594.
Experiments were performed using in vitro perfused medullary thick ascending limbs of Henle (MTAL) and in suspensions of MTAL tubules isolated from mouse kidney to evaluate the effects of arginine vasopressin (AVP) on the K+ dependence of the apical, furosemide-sensitive Na+:Cl- cotransporter and on transport-related oxygen consumption (QO2). In isolated perfused MTAL segments, the rate of cell swelling induced by removing K+ from, and adding one mM ouabain to, the basolateral solution [ouabain(zero-K+)] provided an index to apical cotransporter activity and was used to evaluate the ionic requirements of the apical cotransporter in the presence and absence of AVP. In the absence of AVP cotransporter activity required Na+ and Cl-, but not K+, while the presence of AVP the apical cotransporter required all three ions. 86Rb+ uptake into MTAL tubules in suspension was significant only after exposure of tubules to AVP. Moreover, 22Na+ uptake was unaffected by extracellular K+ in the absence of AVP while after AVP exposure 22Na+ uptake was strictly K(+)-dependent. The AVP-induced coupling of K+ to the Na+:Cl- cotransporter resulted in a doubling in the rate of NaCl absorption without a parallel increase in the rate of cellular 22Na+ uptake or transport-related oxygen consumption. These results indicate that arginine vasopressin alters the mode of a loop diuretic-sensitive transporter from Na+: Cl- cotransport to Na+: K+: 2Cl- cotransport in the mouse MTAL with the latter providing a distinct metabolic advantage for sodium transport. A model for AVP action on NaCl absorption by the MTAL is presented and the physiological significance of the coupling of K+ to the apical Na+: Cl- cotransporter in the MTAL and of the enhanced metabolic efficiency are discussed.
采用体外灌注的髓袢升支粗段（MTAL）以及从小鼠肾脏分离得到的MTAL小管悬浮液进行实验，以评估精氨酸加压素（AVP）对顶端呋塞米敏感的Na⁺:Cl⁻共转运体的钾依赖性以及对转运相关耗氧量（QO₂）的影响。在分离的灌注MTAL节段中，通过从基底外侧溶液中去除钾离子并添加1 mM哇巴因[哇巴因（零钾）]诱导的细胞肿胀速率提供了顶端共转运体活性的指标，并用于评估在有或没有AVP存在时顶端共转运体的离子需求。在没有AVP的情况下，共转运体活性需要Na⁺和Cl⁻，但不需要K⁺，而在有AVP存在时，顶端共转运体需要所有三种离子。只有在小管暴露于AVP后，悬浮的MTAL小管中⁸⁶Rb⁺摄取才显著。此外，在没有AVP的情况下，细胞外钾离子不影响²²Na⁺摄取，而在AVP暴露后，²²Na⁺摄取严格依赖于K⁺。AVP诱导的K⁺与Na⁺:Cl⁻共转运体的偶联导致NaCl吸收速率加倍，而细胞²²Na⁺摄取速率或转运相关耗氧量没有相应增加。这些结果表明，精氨酸加压素改变了小鼠MTAL中一种对袢利尿剂敏感的转运体的模式，从Na⁺:Cl⁻共转运转变为Na⁺:K⁺:2Cl⁻共转运，后者为钠转运提供了独特的代谢优势。本文提出了AVP对MTAL吸收NaCl作用的模型，并讨论了MTAL中K⁺与顶端Na⁺:Cl⁻共转运体偶联以及代谢效率提高的生理意义。
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