Linas S L, Peterson L N, Anderson R J, Aisenbrey G A, Simon F R, Berl T
Kidney Int. 1979 Jun;15(6):601-11. doi: 10.1038/ki.1979.79.
The mechanisms responsible for renal potassium (K) conservation during dietary potassium deficiency are poorly understood. This study was undertaken to investigate the time course of potassium conservation as well as the roles of distal sodium (Na) delivery, the distal delivery or sodium plus a nonpermeable anion, mineralocorticoid hormone, renal tissue potassium content, and Na-K-ATPase activity in renal potassium conservation. After 72 hours of a low-potassium diet, basal potassium excretion was negligible. After 24 hours, and even more so after 72 hours of potassium restriction, the kaliuretic response to increasing distal delivery of sodium or sodium plus a nonpermeable anion was impaired. After 24 hours of a low-potassium diet, plasma aldosterone levels fell from 180 +/- 25 to 32 +/- 9 pg/ml (P less than 0.001). Mineralocorticoid hormone given in the first 24 hours of a low-potassium diet resulted in a greater potassium loss (1564 +/- 125 muEq) than it did in controls on the same diet not receiving mineralocorticoid hormone (1032 +/- 83 muEq, P less than 0.005). In contrast, after 72 hours of diet, large doses of mineralocorticoid hormone failed to cause a kaliuresis in either anesthetized or conscious rats. After both 24 and 72 hours, outer medullary Na-K-ATPase was increased. At 72 hours, cortical, medullary, and papillary tissue potassium concentrations were significantly depressed. Acute administration of potassium repleted tissue potassium levels and restored basal and saline-stimulated potassium excretion to normal. Although potassium excretion was markedly depressed after 24 hours of the low-potassium diet, 42K microinjection studies of the distal nephron did not suggest any increase in potassium reabsorption. Following 72 hours of diet, potassium reabsorption increased significantly from 26 +/- 2% to 41 +/- 2% (P less than 0.001). We conclude that renal potassium conservation is at first primarily related to a decrease in potassium secretion, which is most likely mediated by falling levels of mineralocorticoid hormone. After 72 hours of the potassium-deficient diet, however, potassium conservation becomes independent of mineralocorticoid hormone, distal delivery of sodium, and Na-K-ATPase. The decreased tissue potassium content appears to be the primary mediator of both the increase in potassium reabsorption by the distal nephron and of renal potassium conservation at this time.
饮食中钾缺乏时肾脏保钾的机制尚不清楚。本研究旨在探讨保钾的时间进程，以及远端钠（Na）输送、远端钠加不可渗透阴离子的输送、盐皮质激素、肾组织钾含量和Na-K-ATP酶活性在肾脏保钾中的作用。低钾饮食72小时后，基础钾排泄可忽略不计。钾限制24小时后，尤其是72小时后，对增加远端钠或钠加不可渗透阴离子输送的利钾反应受损。低钾饮食24小时后，血浆醛固酮水平从180±25降至32±9 pg/ml（P<0.001）。低钾饮食的前24小时给予盐皮质激素导致的钾丢失（1564±125 μEq）比未接受盐皮质激素的相同饮食对照组（1032±83 μEq，P<0.005）更多。相反，饮食72小时后，大剂量盐皮质激素在麻醉或清醒大鼠中均未能引起利钾作用。24小时和72小时后，外髓质Na-K-ATP酶均增加。72小时时，皮质、髓质和乳头组织钾浓度显著降低。急性补钾可使组织钾水平恢复，并使基础和盐水刺激的钾排泄恢复正常。尽管低钾饮食24小时后钾排泄明显减少，但对远端肾单位的42K微量注射研究未提示钾重吸收增加。饮食72小时后，钾重吸收从26±2%显著增加至41±2%（P<0.001）。我们得出结论，肾脏保钾起初主要与钾分泌减少有关，这很可能是由盐皮质激素水平下降介导的。然而，低钾饮食72小时后，保钾变得独立于盐皮质激素、远端钠输送和Na-K-ATP酶。此时，组织钾含量降低似乎是远端肾单位钾重吸收增加和肾脏保钾的主要介导因素。
