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10.1152/ajprenal.00015.2014

http://scihub22266oqcxt.onion/10.1152/ajprenal.00015.2014
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suck abstract from ncbi

pmid24598799      Am+J+Physiol+Renal+Physiol 2014 ; 306 (9): F1059-68
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  • Increasing plasma K+ by intravenous potassium infusion reduces NCC phosphorylation and drives kaliuresis and natriuresis #MMPMID24598799
  • Rengarajan S; Lee DH; Oh YT; Delpire E; Youn JH; McDonough AA
  • Am J Physiol Renal Physiol 2014[May]; 306 (9): F1059-68 PMID24598799show ga
  • 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.
  • |*Natriuresis[MESH]
  • |Animals[MESH]
  • |Disease Models, Animal[MESH]
  • |Epithelial Sodium Channels/metabolism[MESH]
  • |Hyperkalemia/*blood/chemically induced/physiopathology/urine[MESH]
  • |Infusions, Intravenous[MESH]
  • |Kidney/*metabolism/physiopathology[MESH]
  • |Male[MESH]
  • |Phosphorylation[MESH]
  • |Potassium Channels/metabolism[MESH]
  • |Potassium, Dietary/blood/urine[MESH]
  • |Potassium/administration & dosage/*blood/urine[MESH]
  • |Protein Serine-Threonine Kinases/metabolism[MESH]
  • |Rats[MESH]
  • |Rats, Sprague-Dawley[MESH]
  • |Sodium-Hydrogen Exchanger 3[MESH]
  • |Sodium-Hydrogen Exchangers/metabolism[MESH]
  • |Sodium/blood/*urine[MESH]
  • |Solute Carrier Family 12, Member 3/metabolism[MESH]


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