Application of Potassium Ion Deposition in Determining the Impact of Support Reducibility on Catalytic Activity of Au/Ceria-Zirconia Catalysts in CO Oxidation, NO Oxidation, and C3H8 Combustion

The purpose of the study was to show how a controlled, subtle change of the reducibility of the support by deposition of potassium ions impacts the activity of gold catalysts. Since the activity of supported gold catalysts in carbon monoxide oxidation is known to strongly depend on the reducibility of the support, this reaction was chosen as the model reaction. The results of tests conducted in a simple system in which the only reagents were CO and O2 showed good agreement with the CO activity trend in tests performed in a complex stream of reagents, which also contained CH4, C2H6, C3H8, NO, and water vapor. The results of the X-ray Diffraction (XRD) studies revealed that the support has the composition Ce0.85Zr0.15O2, that its lattice constant is the same for all samples, and that gold is mostly present in the metallic phase. The reducibility of the systems was established based on Temperature Programmed Reduction (TPR) and in situ XRD measurements in H2 atmosphere. The results show that the low temperature reduction peak, which is due to the presence of gold, is shifted to a higher value by the presence of 0.3 at% potassium ions on the surface. Moreover, the increase of the potassium loading leads to a more pronounced shift. The T50 of CO oxidation in the simple model stream was found to exhibit an excellent linear correlation with the maximum temperature of the low temperature reduction peak of Au catalysts. This means that stabilizing oxygen with a known amount of potassium ions can be numerically used to estimate the T50 in CO oxidation. The results in the complex stream also showed a similar dependence of CO conversion on reducibility, though there was no substantial difference in the activity of the catalysts in other reactions regardless of the potassium loading. These studies have shown that the influence of potassium varies depending on the reaction, which highlights differences in the impact of reducibility and importance of other factors in these reactions.

Potassium-regulated distal tubule WNK bodies are kidney-specific WNK1 dependent

With-no-lysine (WNK) kinases coordinate volume and potassium homeostasis by regulating renal tubular electrolyte transport. In the distal convoluted tubule (DCT), potassium imbalance causes WNK signaling complexes to concentrate into large discrete foci, which we call “WNK bodies.” Although these structures have been reported previously, the mechanisms that drive their assembly remain obscure. Here, we show that kidney-specific WNK1 (KS-WNK1), a truncated kinase-defective WNK1 isoform that is highly expressed in the DCT, is critical for WNK body formation. While morphologically distinct WNK bodies were evident in the distal tubules of mice subjected to dietary potassium loading and restriction, KS-WNK1 knockout mice were deficient in these structures under identical conditions. Combining in vivo observations in kidney with reconstitution studies in cell culture, we found that WNK bodies are dynamic membraneless foci that are distinct from conventional organelles, colocalize with the ribosomal protein L22, and cluster the WNK signaling pathway. The formation of WNK bodies requires an evolutionarily conserved cysteine-rich hydrophobic motif harbored within a unique N-terminal exon of KS-WNK1. We propose that WNK bodies are not pathological aggregates, but rather are KS-WNK1–dependent microdomains of the DCT cytosol that modulate WNK signaling during physiological shifts in potassium balance.

Increasing plasma [K+] by intravenous potassium infusion reduces NCC phosphorylation and drives kaliuresis and natriuresis

Dietary potassium loading results in rapid kaliuresis, natriuresis, and diuresis associated with reduced phosphorylation (p) of the distal tubule Na+-Cl− cotransporter (NCC). Decreased NCC-p inhibits NCC-mediated Na+ reabsorption and shifts Na+ downstream for reabsorption by epithelial Na+ channels (ENaC), which can drive K+ secretion. Whether the signal is initiated by ingesting potassium or a rise in plasma K+ concentration ([K+]) is not understood. We tested the hypothesis, in male rats, that an increase in plasma [K+] is sufficient to reduce NCC-p and drive kaliuresis. After an overnight fast, a single 3-h 2% potassium (2%K) containing meal increased plasma [K+] from 4.0 ± 0.1 to 5.2 ± 0.2 mM; increased urinary K+, Na+, and volume excretion; decreased NCC-p by 60%; and marginally reduced cortical Na+-K+-2Cl− cotransporter (NKCC) phosphorylation 25% ( P = 0.055). When plasma [K+] was increased by tail vein infusion of KCl to 5.5 ± 0.1 mM over 3 h, significant kaliuresis and natriuresis ensued, NCC-p decreased by 60%, and STE20/SPS1-related proline alanine-rich kinase (SPAK) phosphorylation was marginally reduced 35% ( P = 0.052). The following were unchanged at 3 h by either the potassium-rich meal or KCl infusion: Na+/H+ exchanger 3 (NHE3), NHE3-p, NKCC, ENaC subunits, and renal outer medullary K+ channel. In summary, raising plasma [K+] by intravenous infusion to a level equivalent to that observed after a single potassium-rich meal triggers renal kaliuretic and natriuretic responses, independent of K+ ingestion, likely driven by decreased NCC-p and activity sufficient to shift sodium reabsorption downstream to where Na+ reabsorption and flow drive K+ secretion.