The distal convoluted tubule (DCT) of the kidney plays an important role in blood pressure regulation by modulating Na+ reabsorption via the Na+-Cl- cotransporter (NCC). A diet containing high salt (NaCl) and low K+ activates NCC, thereby causing Na+ retention and a rise in blood pressure. Since high blood pressure, hypertension, is associated with changes in serum calcium (Ca2+) and magnesium (Mg2+) levels, we hypothesized that dietary Na+ and K+ intake affects Ca2+ and Mg2+ transport in the DCT. Therefore, the present study aimed to investigate the effect of a high-Na+/low-K+ diet on renal Ca2+ and Mg2+ handling. Mice were divided in four groups and fed a normal-Na+/normal-K+, normal-Na+/low-K+, high-Na+/normal-K+, or high- Na+/low-K+ diet for 4 days. Serum and urine were collected for electrolyte and hormone analysis. Gene and protein expression of electrolyte transporters were assessed in kidney and intestine by qPCR and immunoblotting. Whereas Mg2+ homeostasis was not affected, the mice had elevated urinary Ca2+ and phosphate (Pi) excretion upon high Na+ intake, as well as significantly lower serum Ca2+ levels in the high-Na+/low-K+ group. Alterations in the gene and protein expression of players involved in Ca2+ and Pi transport indicate that reabsorption in the proximal tubular and TAL is affected, while inducing a compensatory response in the DCT. These effects may contribute to the negative health impact of a high-salt diet, including kidney stone formation, chronic kidney disease, and loss of bone mineral density.

Additional Metadata
Keywords Calcium, Kidney, Phosphate, Potassium, Salt
Persistent URL dx.doi.org/10.1152/ajprenal.00379.2017, hdl.handle.net/1765/114065
Journal American Journal of Physiology - Renal Fluid and Electrolyte Physiology
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Citation
van der Wijst, J, Tutakhel, O.A.Z, Bos, C, Danser, A.H.J, Hoorn, E.J, Hoenderop, J.G.J, & Bindels, R.J.M. (2018). Effects of a high-sodium/low-potassium diet on renal calcium, magnesium, and phosphate handling. American Journal of Physiology - Renal Fluid and Electrolyte Physiology, 315(1), F110–F122. doi:10.1152/ajprenal.00379.2017