Department of Cell and Neurobiology, Keck School of Medicine of University of Southern California, Los Angeles, California, USA.
Am J Physiol Renal Physiol. 2012 Jul 1;303(1):F92-104. doi: 10.1152/ajprenal.00032.2012. Epub 2012 Apr 11.
Dietary potassium (K(+)) restriction and hypokalemia have been reported to change the abundance of most renal Na(+) and K(+) transporters and aquaporin-2 isoform, but results have not been consistent. The aim of this study was to reexamine Na(+), K(+) and H(2)O transporters' pool size regulation in response to removing K(+) from a diet containing 0.74% NaCl, as well as from a diet containing 2% NaCl (as found in American diets) to blunt reducing total diet electrolytes. Sprague-Dawley rats (n = 5-6) were fed for 6 days with one of these diets: 2% KCl, 0.74% NaCl (2K1Na, control chow) compared with 0.03% KCl, 0.74% NaCl (0K1Na); or 2% KCl, 2%NaCl (2K2Na) compared with 0.03% KCl, 2% NaCl (0K2Na, Na(+) replete). In both 0K1Na and 0K2Na there were significant decreases in: 1) plasma [K(+)] (<2.5 mM); 2) urinary K(+) excretion (<5% of control); 3) urine osmolality and plasma [aldosterone], as well as 4) an increase in urine volume and medullary hypertrophy. The 0K2Na group had the lowest [aldosterone] (172.0 ± 17.4 pg/ml) and lower blood pressure (93.2 ± 4.9 vs. 112.0 ± 3.1 mmHg in 2K2Na). Transporter pool size regulation was determined by quantitative immunoblotting of renal cortex and medulla homogenates. The only differences measured in both 0K1Na and 0K2Na groups were a 20-30% decrease in cortical β-ENaC, 30-40% increases in kidney-specific Ste20/SPS1-related proline/alanine-rich kinase, and a 40% increase in medullary sodium pump abundance. The following proteins were not significantly changed in both the 0 K groups: Na(+)/H(+) exchanger isoform 3; Na(+)-K(+)-Cl(-) cotransporter; Na(+)-Cl(-) cotransporter, oxidative stress response kinase-1; renal outer medullary K(+) channel; autosomal recessive hypercholesterolemia; c-Src, aquaporin 2 isoform; or renin. Thus, despite profound hypokalemia and renal K(+) conservation, we did not confirm many of the changes that were previously reported. We predict that changes in transporter distribution and activity are likely more important for conserving K(+) than changes in total abundance.
饮食钾（K(+））限制和低钾血症已被报道会改变大多数肾脏 Na(+) 和 K(+) 转运体和水通道蛋白-2 同工型的丰度，但结果并不一致。本研究的目的是重新检查 Na(+)、K(+) 和 H(2)O 转运体的池大小调节，以响应从含有 0.74%NaCl 的饮食中去除 K(+)，以及从含有 2%NaCl（如美国饮食中发现的）的饮食中去除 K(+)，以减轻总饮食电解质。Sprague-Dawley 大鼠（n = 5-6）用以下饮食之一喂养 6 天：2%KCl，0.74%NaCl（2K1Na，对照饲料）与 0.03%KCl，0.74%NaCl（0K1Na）；或 2%KCl，2%NaCl（2K2Na）与 0.03%KCl，2%NaCl（0K2Na，Na(+) 充足）。在 0K1Na 和 0K2Na 中均有以下明显变化：1）血浆[K(+)]（<2.5mM）；2）尿 K(+)排泄量（<对照的 5%）；3）尿渗透压和血浆[醛固酮]，以及 4）尿量增加和髓质肥大。0K2Na 组的[醛固酮]最低（172.0 ± 17.4 pg/ml），血压也最低（93.2 ± 4.9 与 2K2Na 中的 112.0 ± 3.1mmHg）。转运体池大小调节通过定量免疫印迹法测定肾皮质和髓质匀浆。在 0K1Na 和 0K2Na 组中仅测量到以下差异：皮质β-ENaC 减少 20-30%，肾脏特异性 Ste20/SPS1 相关脯氨酸/丙氨酸丰富激酶增加 30-40%，髓质钠泵丰度增加 40%。在这两个 0K 组中，以下蛋白质均无明显变化：Na(+) / H(+)交换体同工型 3；Na(+) - K(+) - Cl(-)共转运体；Na(+) - Cl(-)共转运体，氧化应激反应激酶-1；肾外髓质 K(+)通道；常染色体隐性高胆固醇血症；c-Src，水通道蛋白 2 同工型；或肾素。因此，尽管低钾血症和肾脏 K(+) 储存严重，但我们并未证实以前报道的许多变化。我们预测，转运体分布和活性的变化可能比总丰度的变化更重要，更有利于 K(+)的储存。
