ArticleKidney international2011
Angiotensin II: a candidate for an aldosterone-independent mediator of potassium preservation during volume depletion.
Article in Kidney international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Two Mineralocorticoid Receptor-Mediated Mechanisms of Pendrin Activation in Distal Nephrons.Journal of the American Society of Nephrology : JASN · 2020Article
- The sodium chloride cotransporter SLC12A3: new roles in sodium, potassium, and blood pressure regulation.Pflugers Archiv : European journal of physiology · 2014Review
- Aldosterone does not require angiotensin II to activate NCC through a WNK4-SPAK-dependent pathway.Pflugers Archiv : European journal of physiology · 2012Article
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Abstract
Two different stimulators of aldosterone secretion, high-potassium diet and low-sodium diet, have disparate effects on potassium secretion in the distal nephron. The mechanism by which the kidney preserves potassium in the face of a high-aldosterone, volume-depleted state has engendered much thought. Yue et al. now propose that angiotensin II inhibits the renal outer medullary potassium channel (ROMK1) through stimulation of the protein tyrosine kinase c-Src, perhaps acting as a signal to differentiate volume depletion from a high-potassium diet.
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