ArticleHypertension (Dallas, Tex. : 1979)2016
Potassium Supplementation Prevents Sodium Chloride Cotransporter Stimulation During Angiotensin II Hypertension.
Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 48 citations in OpenAlex.
- Sex and race differences in urinary Tumor Necrosis Factor-α (TNF-α) levels: Secondary analysis of the DASH-sodium trial.Journal of human hypertension · 2023Trial
- Trial
- The kidney distal tubule potassium switch, modern diet and hypertension.Nature reviews. Nephrology · 2026Review
- Sexual dimorphic pattern of renal transporters and channels in spontaneously hypertensive rats.American journal of physiology. Cell physiology · 2026Article
- Quantitative analysis of skeletal muscle contributions to ECF KAmerican journal of physiology. Cell physiology · 2026Review
- The exquisite link between potassium homeostasis regulation and cardiovascular health: exploration and analysis.Frontiers in physiology · 2026Review
- Sodium Chloride Cotransporter in Hypertension.Biomedicines · 2024Review
- Angiotensin II-Type-1a Receptor and Renal K + Wasting during Overnight Low-Na + Intake.Journal of the American Society of Nephrology : JASN · 2024Article
- Role of calcineurin in regulating renal potassium (KActa physiologica (Oxford, England) · 2024Review
- Role of Angiotensin II Type 1a Receptor (AT1aR) of Renal Tubules in Regulating Inwardly Rectifying Potassium Channels 4.2 (Kir4.2), Kir4.1, and Epithelial NaHypertension (Dallas, Tex. : 1979) · 2024Article
- Angiotensin II hypertension along the female rat tubule: predicted impact on coupled transport of NaAmerican journal of physiology. Renal physiology · 2023Article
- Thirty years of the NaCl cotransporter: from cloning to physiology and structure.American journal of physiology. Renal physiology · 2023Review
- Blood pressure effects of sodium transport along the distal nephron.Kidney international · 2022Review
- In Primary Aldosteronism Acute Potassium Chloride Supplementation Suppresses Abundance and Phosphorylation of the Sodium-Chloride Cotransporter.Kidney360 · 2022Article
- Potassium homeostasis: sensors, mediators, and targets.Pflugers Archiv : European journal of physiology · 2022Review
- Effects of enriched-potassium diet on cardiorespiratory outcomes in experimental non-ischemic chronic heart failure.Biological research · 2021Article
- Dietary potassium and the kidney: lifesaving physiology.Clinical kidney journal · 2020Review
- Osmotic Adaptation by NaBiomedicines · 2020Review
- Coordinate adaptations of skeletal muscle and kidney to maintain extracellular [KAmerican journal of physiology. Cell physiology · 2020Article
- Electrolyte and transporter responses to angiotensin II induced hypertension in female and male rats and mice.Acta physiologica (Oxford, England) · 2020Article
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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<0.05), suggesting that AngII-mediated epithelial Na(+) 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<0.05). The rise in NCC and NCCp abundance was prevented in the A2K rats, yet blood pressure did not significantly decrease. Epithelial Na(+) 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.
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