ArticleClinical science (London, England : 1979)2019
Relationship between the renin-angiotensin-aldosterone system and renal Kir5.1 channels.
Article in Clinical science (London, England : 1979), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Molecular Deconstruction of the Medullary Raphe Magnus in the rat: Transcriptional Responses to Repeated Seizures.bioRxiv : the preprint server for biology · 2026Article
- Chronic β-Blockade and Systemic Homeostasis: Molecular Integration of Cardiorenal and Immune Pathways, a Narrative Review.Biomolecules · 2025Review
- Potassium supplementation and depletion during development of salt-sensitive hypertension in male and female SS rats.JCI insight · 2025Article
- Role of KThe American journal of pathology · 2025Article
- Deletion ofiScience · 2024Article
- Characterization of a novel variant in KCNJ16, encoding KPhysiological reports · 2024Article
- Diverse functions of the inward-rectifying potassium channel Kir5.1 and its relationship with human diseases.Frontiers in physiology · 2023Review
- Kir5.1 channels: potential role in epilepsy and seizure disorders.American journal of physiology. Cell physiology · 2022Review
- Accelerated lysine metabolism conveys kidney protection in salt-sensitive hypertension.Nature communications · 2022Article
- SGLT2 inhibition effect on salt-induced hypertension, RAAS, and NaAmerican journal of physiology. Renal physiology · 2022Article
- Crosstalk between epithelial sodium channels (ENaC) and basolateral potassium channels (KBritish journal of pharmacology · 2022Article
- Pathophysiology and genetics of salt-sensitive hypertension.Frontiers in physiology · 2022Review
- Article
- Expression, localization, and functional properties of inwardly rectifying KAmerican journal of physiology. Renal physiology · 2020Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Kir5.1 (encoded by the Kcnj16 gene) is an inwardly rectifying K+ (Kir) channel highly expressed in the aldosterone-sensitive distal nephron of the kidney, where it forms a functional channel with Kir4.1. Kir4.1/Kir5.1 channels are responsible for setting the transepithelial voltage in the distal nephron and collecting ducts and are thereby major determinants of fluid and electrolyte distribution. These channels contribute to renal blood pressure control and have been implicated in salt-sensitive hypertension. However, mechanisms pertaining to the impact of K ir4.1/Kir5.1-mediated K+ transport on the renin-angiotensin-aldosterone system (RAAS) remain unclear. Herein, we utilized a knockout of Kcnj16 in the Dahl salt-sensitive rat (SSKcnj16-/-) to investigate the relationship between Kir5.1 and RAAS balance and function in the sensitivity of blood pressure to the dietary Na+/K+ ratio. The knockout of Kcnj16 caused substantial elevations in plasma RAAS hormones (aldosterone and angiotensin peptides) and altered the RAAS response to changing the dietary Na+/K+ ratio. Blocking aldosterone with spironolactone caused rapid mortality in SSKcnj16-/- rats. Supplementation of the diet with high K+ was protective against mortality resulting from aldosterone-mediated mechanisms. Captopril and losartan treatment had no effect on the survival of SSKcnj16-/- rats. However, neither of these drugs prevented mortality of SSKcnj16-/- rats when switched to high Na+ diet. These studies revealed that the knockout of Kcnj16 markedly altered RAAS regulation and function, suggesting Kir5.1 as a key regulator of the RAAS, particularly when exposed to changes in dietary sodium and potassium content.
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