Wingo C S, Seldin D W, Kokko J P, Jacobson H R
J Clin Invest. 1982 Sep;70(3):579-86. doi: 10.1172/jci110650.
Addisonian patients can maintain potassium homeostasis despite the absence of mineralocorticoid. The present in vitro microperfusion studies examine what role the cortical collecting tubule might play in this process. All studies were performed on tubules harvested from adrenalectomized rabbits, which were maintained on 0.15 M NaCl drinking water and dexamethasone 50 mug/d. Perfusion and bath solutions were symmetrical Ringer's bicarbonate with [K] of 5 meq/liter. Initial studies on cortical collecting tubules from adrenalectomized animals ingesting a high potassium chow (9 meq K/kg body wt) demonstrated net potassium secretion against an electrochemical gradient (mean collected fluid [K] 16.5+/-2.6 meq/liter with an observed transepithelial voltage of -6.3+/-4.1 mV; predicted voltage for passive distribution of potassium being -28.2 mV). To examine whether this active potassium secretion could be modulated by dietary potassium, independent of mineralocorticoid, two diets identical in all respects except for potassium content were formulated. Potassium secretion was compared in cortical collecting tubules harvested from adrenalectomized animals on low (0.1 meq K) and high (10 meq K) potassium intake. Mean net potassium secretion by cortical collecting tubules was 2.02+/-0.54 peq mm(-1) min(-1) in the low potassium diet group and 5.34+/-.74 peq.mm(-1).min(-1) in the high potassium group. The mean transepithelial voltages of the collecting tubules did not differ between the two dietary groups. While net Na reabsorption was significantly greater in tubules from the high K group, this could not account for the differences in K secretion. These data demonstrate that: (a) the cortical collecting tubule can actively secrete potassium and that the magnitude of this potassium secretion correlates with potassium intake; (b) this active potassium secretory process in independent of mineralocorticoid. These findings support the hypothesis that the cortical collecting tubule may contribute to K homeostasis in Addison's disease.
艾迪生病患者在缺乏盐皮质激素的情况下仍能维持钾稳态。目前的体外微灌注研究探讨了皮质集合管在这一过程中可能发挥的作用。所有研究均在取自肾上腺切除兔子的肾小管上进行，这些兔子饮用含0.15M氯化钠的水并每日给予50微克地塞米松。灌注液和浴液均为对称的含5毫当量/升[K]的林格氏碳酸氢盐溶液。对摄入高钾食物（9毫当量钾/千克体重）的肾上腺切除动物的皮质集合管进行的初步研究表明，钾可逆电化学梯度进行净分泌（收集液中钾的平均浓度为16.5±2.6毫当量/升，观察到的跨上皮电压为-6.3±4.1毫伏；钾被动分布的预测电压为-28.2毫伏）。为了研究这种主动钾分泌是否可受饮食钾调节而与盐皮质激素无关，配制了除钾含量外其他方面均相同的两种饮食。比较了取自低（0.1毫当量钾）钾摄入和高（10毫当量钾）钾摄入的肾上腺切除动物的皮质集合管中的钾分泌情况。低钾饮食组皮质集合管的平均净钾分泌为2.02±0.54皮克/毫米(-1)·分钟(-1)，高钾组为5.34±0.74皮克/毫米(-1)·分钟(-1)。两个饮食组的集合管平均跨上皮电压无差异。虽然高钾组肾小管的净钠重吸收明显更多，但这并不能解释钾分泌的差异。这些数据表明：(a)皮质集合管可主动分泌钾，且这种钾分泌的幅度与钾摄入量相关；(b)这种主动钾分泌过程与盐皮质激素无关。这些发现支持了皮质集合管可能有助于艾迪生病患者钾稳态的假说。
