Title : Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4.1 potassium channel.

Pub. Date : 2018 Apr

PMID : 29310825






11 Functional Relationships(s)
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1 Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4.1 potassium channel. Potassium potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus
2 Kir4.1 in the distal convoluted tubule plays a key role in sensing plasma potassium and in modulating the thiazide-sensitive sodium-chloride cotransporter (NCC). Potassium potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus
3 High potassium intake inhibited the basolateral 40 pS potassium channel (a Kir4.1/5.1 heterotetramer) in the distal convoluted tubule, decreased basolateral potassium conductance, and depolarized the distal convoluted tubule membrane in Kcnj10flox/flox mice, herein referred to as control mice. Potassium potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus
4 High potassium intake inhibited the basolateral 40 pS potassium channel (a Kir4.1/5.1 heterotetramer) in the distal convoluted tubule, decreased basolateral potassium conductance, and depolarized the distal convoluted tubule membrane in Kcnj10flox/flox mice, herein referred to as control mice. Potassium potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus
5 High potassium intake inhibited the basolateral 40 pS potassium channel (a Kir4.1/5.1 heterotetramer) in the distal convoluted tubule, decreased basolateral potassium conductance, and depolarized the distal convoluted tubule membrane in Kcnj10flox/flox mice, herein referred to as control mice. Potassium potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus
6 In contrast, low potassium intake activated Kir4.1, increased potassium currents, and hyperpolarized the distal convoluted tubule membrane. Potassium potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus
7 These effects of dietary potassium intake on the basolateral potassium conductance and membrane potential in the distal convoluted tubule were completely absent in inducible kidney-specific Kir4.1 knockout mice. Potassium potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus
8 Finally, hypokalemia and metabolic alkalosis in kidney-specific Kir4.1 knockout mice were exacerbated by potassium restriction and only partially corrected by a high-potassium diet. Potassium potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus
9 Finally, hypokalemia and metabolic alkalosis in kidney-specific Kir4.1 knockout mice were exacerbated by potassium restriction and only partially corrected by a high-potassium diet. Potassium potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus
10 Thus, Kir4.1 plays an essential role in mediating the effect of dietary potassium intake on NCC activity and potassium homeostasis. Potassium potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus
11 Thus, Kir4.1 plays an essential role in mediating the effect of dietary potassium intake on NCC activity and potassium homeostasis. Potassium potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus