Kiil F, Hartmann A, Langberg H, Sejersted O M, Holthe M R
J Pharmacol Exp Ther. 1986 Jul;238(1):327-33.
To examine whether the adenosine triphosphatase (Na,K-ATPase) transport rate regulates transcellular NaCl reabsorption, experiments were performed on anesthetized volume-expanded dogs. Ouabain was injected into the renal artery in doses inhibiting 10 to 80% of the renal Na,K-ATPase activity. Acetazolamide was administered before ouabain to render the NaHCO3 reabsorption and associated NaCl reabsorption constant during variations in the glomerular filtration rate. Ouabain reduced sodium reabsorption significantly after inhibiting 20% of the Na,K-ATPase. By inhibiting 80% of the Na,K-ATPase, NaCl reabsorption was reduced by 40 to 50% without affecting NaHCO3 reabsorption. During mechanical constriction of the suprarenal aorta, the remaining NaCl reabsorption was constant until the glomerular filtration rate was lowered by about 50%. Bound ouabain and the remaining Na,K-ATPase activity were distributed between the cortex and medulla in proportion to the Na,K-ATPase activity before ouabain injection. The reduction in NaCl reabsorption and ouabain binding were correlated (r = 0.90), the slope suggesting a turnover for ATP similar to the in vitro turnover of 5700 ATP min-1 estimated from the relationship between the remaining Na,K-ATPase activity and bound ouabain (r = 0.95). We conclude that transcellular reabsorption of NaCl in the distal nephron reaches a maximum in volume-expanded dogs by saturating the sodium sites of Na,K-ATPase because even a small dose of ouabain inhibits NaCl reabsorption and because the calculated turnover for Na,K-ATPase activity is similar to in vitro maximum estimates. The Na,K-ATPase transport rate, therefore, limits transcellular NaCl reabsorption in volume-expanded dogs.
为研究三磷酸腺苷酶（钠钾 - 三磷酸腺苷酶，Na，K - ATPase）转运速率是否调节跨细胞氯化钠重吸收，我们对麻醉状态下血容量扩充的犬进行了实验。以抑制肾Na，K - ATPase活性10%至80%的剂量将哇巴因注入肾动脉。在注射哇巴因前给予乙酰唑胺，以使在肾小球滤过率变化期间碳酸氢钠重吸收及相关的氯化钠重吸收保持恒定。哇巴因抑制20%的Na，K - ATPase后，钠重吸收显著降低。抑制80%的Na，K - ATPase时，氯化钠重吸收降低40%至50%，而不影响碳酸氢钠重吸收。在机械性收缩肾上腺主动脉期间，剩余的氯化钠重吸收保持恒定，直至肾小球滤过率降低约50%。结合的哇巴因和剩余的Na，K - ATPase活性按哇巴因注射前Na，K - ATPase活性的比例分布于皮质和髓质之间。氯化钠重吸收的降低与哇巴因结合相关（r = 0.90），斜率表明ATP的周转率类似于根据剩余的Na，K - ATPase活性与结合的哇巴因之间的关系估计的体外周转率5700 ATP·min⁻¹（r = 0.95）。我们得出结论，在血容量扩充的犬中，远端肾单位中氯化钠的跨细胞重吸收通过使Na，K - ATPase的钠位点饱和而达到最大值，这是因为即使小剂量的哇巴因也会抑制氯化钠重吸收，并且因为计算出的Na，K - ATPase活性周转率类似于体外最大估计值。因此，在血容量扩充的犬中，Na，K - ATPase转运速率限制了跨细胞氯化钠重吸收。
