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Potassium Supplementation Prevents Sodium Chloride Cotransporter Stimulation During Angiotensin II Hypertension

Authors :
Luciana C. Veiras
Alicia A. McDonough
Jiyang Han
Donna L. Ralph
Source :
Hypertension. 68:904-912
Publication Year :
2016
Publisher :
Ovid Technologies (Wolters Kluwer Health), 2016.

Abstract

Angiotensin II (AngII) hypertension increases distal tubule Na-Cl cotransporter (NCC) abundance and phosphorylation (NCCp), as well as epithelial Na + channel abundance and activating cleavage. Acutely raising plasma [K + ] by infusion or ingestion provokes a rapid decrease in NCCp that drives a compensatory kaliuresis. The first aim tested whether acutely raising plasma [K + ] with a single 3-hour 2% potassium meal would lower NCCp in Sprague–Dawley rats after 14 days of AngII (400 ng/kg per minute). The potassium-rich meal neither decreased NCCp nor increased K + excretion. AngII-infused rats exhibited lower plasma [K + ] versus controls (3.6±0.2 versus 4.5±0.1 mmol/L; P + channel activation provokes K + depletion. The second aim tested whether doubling dietary potassium intake from 1% (A1K) to 2% (A2K) would prevent K + depletion during AngII infusion and, thus, prevent NCC accumulation. A2K-fed rats exhibited normal plasma [K + ] and 2-fold higher K + excretion and plasma [aldosterone] versus A1K. In A1K rats, NCC, NCCpS71, and NCCpT53 abundance increased 1.5- to 3-fold versus controls ( P + channel subunit abundance and cleavage increased 1.5- to 3-fold in both A1K and A2K; ROMK (renal outer medulla K + channel abundance) abundance was unaffected by AngII or dietary K + . In summary, the accumulation and phosphorylation of NCC seen during chronic AngII infusion hypertension is likely secondary to potassium deficiency driven by epithelial Na + channel stimulation.

Details

ISSN :
15244563 and 0194911X
Volume :
68
Database :
OpenAIRE
Journal :
Hypertension
Accession number :
edsair.doi.dedup.....120c07fdf711e5ac384ea501ecf4b544
Full Text :
https://doi.org/10.1161/hypertensionaha.116.07389