Markovich D, Wang H, Puttaparthi K, Zajicek H, Rogers T, Murer H, Biber J, Levi M
Department of Physiology and Pharmacology, University of Queensland, Australia; Institute of Physiology, University of Zurich, Zurich, Switzerland.
Kidney Int. 1999 Jan;55(1):244-51. doi: 10.1046/j.1523-1755.1999.00255.x.
The purpose of this study was to determine if dietary potassium (K) deficiency regulates renal proximal tubular sodium gradient-dependent sulfate transport (Na/Si cotransport) in the rat and, furthermore, determine if the regulation takes place at the level of the recently cloned Na/Si cotransport system (NaSi-1). Methods and Results. Rats treated chronically (seven days) with a K-deficient diet had a significant decrease in serum Si levels and an increase in fractional excretion of ultrafilterable Si, which paralleled a significant decrease in brush border membrane (BBM) Na/Si cotransport activity. The decrease in BBM Na/Si cotransport activity was associated with decreases in BBM NaSi-1 protein and renal cortical NaSi-1 mRNA abundance. In addition, in Xenopus oocytes injected with mRNA from kidney cortex slices of K-deficient rats, there was a significant reduction in the induced Na/Si cotransport, whereas there was no alteration in l-leucine uptake, suggesting that in K-deficient rats, there is a specific decrease in functional mRNA encoding the NaSi-1 mRNA.
These findings indicate that chronic K deficiency leads to a reduction in serum Si levels and an increase fractional excretion of Si, and reduces Si reabsorption by down-regulating the expression of the proximal tubular Na/Si-1 cotransporter protein and mRNA.
本研究的目的是确定膳食钾(K)缺乏是否会调节大鼠肾近端小管钠梯度依赖性硫酸盐转运(Na/Si共转运),此外,确定这种调节是否发生在最近克隆的Na/Si共转运系统(NaSi-1)水平。方法与结果。用低钾饮食长期(7天)处理的大鼠血清Si水平显著降低,超滤性Si的分数排泄增加,这与刷状缘膜(BBM)Na/Si共转运活性的显著降低平行。BBM Na/Si共转运活性的降低与BBM NaSi-1蛋白和肾皮质NaSi-1 mRNA丰度的降低有关。此外,在注射了低钾饮食大鼠肾皮质切片mRNA的非洲爪蟾卵母细胞中,诱导的Na/Si共转运显著降低,而L-亮氨酸摄取没有改变,这表明在低钾饮食大鼠中,编码NaSi-1 mRNA的功能性mRNA有特异性降低。
这些发现表明,慢性钾缺乏导致血清Si水平降低和Si分数排泄增加,并通过下调近端小管Na/Si-1共转运蛋白和mRNA的表达来减少Si重吸收。