Dietary modulation of active potassium secretion in the cortical collecting tubule of adrenalectomized rabbits.
Dietary modulation of active potassium secretion in the cortical collecting tubule of adrenalectomized rabbits.
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肾上腺切除兔皮质集合管中活性钾分泌的饮食调节。
DOI：
10.1172/jci110650
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
H. Jacobson
中科院分区：
文献类型：
--
作者：
C. Wingo;D. Seldin;J. Kokko;H. Jacobson
即使没有使用盐皮质激素，爱迪生患者仍能维持钾稳态。目前的体外微灌流研究检测了皮质集合管在这一过程中可能起到的作用。所有研究均取自去肾上腺的兔肾小管，维持在0.15M氯化钠水和地塞米松50mug/d中，灌流和浴液为对称的Ringer‘s碳酸氢盐，[K]为5meq/L。对摄入高钾食物(9MEQ K/kg体重)的肾上腺切除动物的皮质集合管的初步研究表明，相对于电化学梯度(平均收集的液体[K]16.5+/-2.6meq/L，观察到的跨上皮电压为-6.3+/-4.1 mV；预计被动分配钾的电压为-28.2 mV)，净分泌钾。为了检验这种活跃的钾分泌是否可以被日粮中的钾调节，不依赖于盐皮质激素，设计了两种在所有方面都相同的日粮，除了钾含量。比较了低(0.1meq K)和高(10meq K)钾摄入量下肾上腺切除动物皮质集合管的钾分泌。低钾饮食组大鼠皮质集合管的平均净钾分泌量为2.02+/-0.54PEq·mm(-1)·min(-1)，高钾饮食组为5.34+/-0.74peq·mm(-1)·min(-1)。集合管的平均跨上皮电压在两个饮食组之间没有差异。尽管高钾组肾小管对钠的重吸收显著增加，但这不能解释钾分泌的差异。这些数据表明：(A)皮质集合管可以主动分泌钾，并且这种分泌钾的大小与钾的摄入量有关；(B)这种活跃的钾分泌过程不依赖于盐皮质激素。这些发现支持这一假说，即皮质集合管可能有助于爱迪生病的钾稳态。
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.