The kidney in potassium depletion. II. K+ handling by the isolated perfused rat kidney.
The kidney in potassium depletion. II. K+ handling by the isolated perfused rat kidney.
复制标题
肾脏缺钾。
DOI：
10.1152/ajprenal.1987.252.3.f447
复制
发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Katz,AI
中科院分区：
文献类型：
--
作者：
Hayashi,M;Katz,AI
在另一篇文章中，我们报道了缺钾大鼠外髓集合管内条Na~+-K~+-ATPase活性和[~3H]哇巴因结合量的显著增加。为了验证这些动物体内增加的Na+-K+泵数量可能与钾的重吸收有关的假设，我们研究了哇巴因对喂食无钾饮食3wk的大鼠离体肾K排泄的影响。缺钾大鼠的肾脏大量保留钾，排出钾的分数(Fek)和绝对钾排出量都比对照肾脏低约五倍。哇巴因(5 MM)增加了每只缺钾大鼠肾脏中的FeK[平均从8.5%增加到34.4%，P<0.001，平均(4.5mM)灌流液K]；当肾脏灌流低(约2 mM)和高(大于或等于8 mM)钾浓度时，也获得了类似的结果。相比之下，哇巴因在对照肾脏中产生了不同的影响，这取决于灌流液中的钾浓度。在钾缺乏的大鼠，阿米洛利(10(-4)M)不能显著改变钾的排泄，也不能阻断哇巴因诱导的尿钾，这表明后者不是由于远端液体输送增加而导致的分泌增加所致。这些结果为慢性钾缺乏大鼠肾脏对哇巴因敏感钾的重吸收提供了证据，并为在这类动物中观察到的Na+-K+-ATPase升高提供了解释。
In a companion paper we reported a large increment in Na+-K+-ATPase activity and [3H]ouabain binding in the inner stripe of outer medullary collecting tubules from K-depleted rats. To test the hypothesis that the increased number of Na+-K+ pumps in these animals may be involved in potassium reabsorption we examined the effect of ouabain on K excretion by isolated, perfused kidneys from rats fed a K-free diet for 3 wk. Kidneys from K-depleted rats retain potassium avidly, both the fractional (FEK) and absolute K excretion being approximately fivefold lower than in control kidneys. Ouabain (5 mM) increased FEK in kidneys from each K-depleted rat [mean from 8.5 to 34.4%, P less than 0.001, at average (4.5 mM) perfusate K]; similar results were obtained when kidneys were perfused with low (approximately 2 mM) and high (greater than or equal to 8 mM) potassium concentrations. In contrast, ouabain produced a variable effect in control kidneys, that depended on the perfusate potassium concentration. In K-depleted rats amiloride (10(-4) M) did not significantly alter K excretion and did not block the ouabain-induced kaliuresis, suggesting that the latter is not due to enhanced secretion secondary to increased distal fluid delivery. These results provide evidence for ouabain-sensitive potassium reabsorption in kidneys of chronically K-depleted rats, and suggest an explanation for the increased Na+-K+-ATPase observed in such animals.