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Review
. 2016 Apr 1;310(7):F581-F595.
doi: 10.1152/ajprenal.00330.2015. Epub 2016 Jan 6.

Maintaining K+ balance on the low-Na+, high-K+ diet

Ryan J Cornelius  1 , Bangchen Wang  2 , Jun Wang-France  2 , Steven C Sansom  3
Affiliations
Review

Maintaining K+ balance on the low-Na+, high-K+ diet

Ryan J Cornelius et al. Am J Physiol Renal Physiol. .

Abstract

A low-Na+, high-K+ diet (LNaHK) is considered a healthier alternative to the "Western" high-Na+ diet. Because the mechanism for K+ secretion involves Na+ reabsorptive exchange for secreted K+ in the distal nephron, it is not understood how K+ is eliminated with such low Na+ intake. Animals on a LNaHK diet produce an alkaline load, high urinary flows, and markedly elevated plasma ANG II and aldosterone levels to maintain their K+ balance. Recent studies have revealed a potential mechanism involving the actions of alkalosis, urinary flow, elevated ANG II, and aldosterone on two types of K+ channels, renal outer medullary K+ and large-conductance K+ channels, located in principal and intercalated cells. Here, we review these recent advances.

Keywords: Na+-Cl− cotransporter; angiotensin II; epithelial Na+ channel; large-conductance K+ channel; renal outer medullary K+ channel.

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Figures

Fig. 1.
Fig. 1.
Illustration of the effects of acidic or alkaline loading on coordinated transport between prinicpal cells (PCs) and intercalated cells (ICs) of mice on a low-Na+, high-K+ (LNaHK) diet. A: mechanism of HCO3−-promoted K+ secretion in predominant IC-β in the connecting tubule (CNT) of mice on a LNaHK diet. With only IC-β, the reabsorbed Cl− is exchanged for secreted HCO3− via pendrin and the lumen negative potential from Na+ reabsorbed via epithelial Na+ channels (ENaC) drives the secretion of K+ from PCs and ICs. B: mechanism of K+ secretion with the LNaHK-Cl− diet. As the load becomes more acidic, IC-β are converted to IC-α (108, 126) in the CNT and initial cortical collecting duct (CCD). Cl− is reabsorbed via pendrin in exchange for secreted HCO3−, which binds to H+, which is pumped into the lumen from IC-α. CO2 recycles back through IC-β. H2O would recycle back via aquaporin 5, which is localized on IC-β (105), and its apical membrane insertion is linked with K+ intake (106). CO2 and H2O would combine to generate HCO3−, which would be secreted, and H+, which would be actively transported into the plasma via basolateral H+-ATPase. The result is Na+ reabsorption with Cl− rather than exchange with K+. The reduced driving force for K+ secretion is reflected by the lower transtubular K+ gradient and subsequent rise in plasma K+ concentration (P[K+])for mice on an acidic LNaHK diet (Table 1). The urine is acidified in the inner medullary collecting ducts, where the predominating cells are acid secreting IC-α. BK, large-conductance Ca2+-activated K+ channels.
Fig. 2.
Fig. 2.
Cell models illustrating the effects of the LNaHK diet on Na+ and K+ transport properties of the distal nephron. A and B: illustrations of the Na+ and K+ transport pathways of the early distal convoluted tubule (DCT1) and CNT/CCD of animals on a regular diet (A) or LNaHK diet (B). A: for mice on a regular diet, ENaC reabsorbs 50% more Na+ than the Na+-Cl− cotransporter (NCC) in the distal nephron. Approximately 75% of the K+ transported on Na+-K+-ATPase is secreted into the lumen, and 25% is recycled across the basolateral membrane to yield a Na+ reabsorbed-to-K+ secreted ratio of 0.5. Cl− is reabsorbed via pendrin to account for the charge balance with Na+ reabsorption. B: the high K+ intake or elevating P[K+] turns off NCC of the DCT1, increasing the delivery of Na+ to ENaC. Renal and plasma ANG II levels elevate in response to the low Na+ intake with an increase in ENaC open probability and activation of renal outer medullary K+ (ROMK) channels. Aldosterone (Aldo) has several effects to enhance K+ secretion, including increasing BK channels in ICs and Na+-K+-ATPase, ENaC, and ROMK channels in PCs. The elevated flow stimulates BK channels in PCs and ICs. To enhance the secreted K+-to-Na+ reabsorbed ratio greater than 2, it is hypothesized that Na+ is recycled via the Na+-dependent Cl−/HCO3− exchanger.
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