ArticleProceedings of the National Academy of Sciences of the United States of America2005
Aldosterone acts via an ATP autocrine/paracrine system: the Edelman ATP hypothesis revisited.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 61 citations in OpenAlex.
- Development of scanning ion-conductance microscopy based tip-enhanced Raman spectroscopy in liquid environments.Nanotechnology · 2026Review
- Gap Junctional Versus Paracrine Signaling in the Human Lens Epithelium: Analysis Based on Multicellular Ca²⁺ Imaging and Computational Modeling.Investigative ophthalmology & visual science · 2025Article
- P2Y2 receptor decreases blood pressure by inhibiting ENaC.JCI insight · 2023Article
- Scanning Ion Conductance Microscopy.Chemical reviews · 2021Review
- New Horizons: Does Mineralocorticoid Receptor Activation by Cortisol Cause ATP Release and COVID-19 Complications?The Journal of clinical endocrinology and metabolism · 2021Article
- P2X7 Receptors: An Untapped Target for the Management of Cardiovascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Follow Your Nose: A Key Clue to Understanding and Treating COVID-19.Frontiers in endocrinology · 2021Article
- The renal and blood pressure response to low sodium diet in P2X4 receptor knockout mice.Physiological reports · 2018Article
- Angular Approach Scanning Ion Conductance Microscopy.Biophysical journal · 2016Article
- Article
- Salt controls endothelial and vascular phenotype.Pflugers Archiv : European journal of physiology · 2015Review
- Basolateral P2X₄channels stimulate ENaC activity in Xenopus cortical collecting duct A6 cells.American journal of physiology. Renal physiology · 2014Article
- Feedforward activation of endothelial ENaC by high sodium.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Phosphoinositide 3-kinase pathway mediates early aldosterone action on morphology and epithelial sodium channel in mammalian renal epithelia.The Journal of membrane biology · 2014Article
- Purinergic signalling in the kidney in health and disease.Purinergic signalling · 2014Review
- Characterization of two mammalian cortical collecting duct cell lines with hopping probe ion conductance microscopy.The Journal of membrane biology · 2013Article
- The relationship between P2X4 and P2X7: a physiologically important interaction?Frontiers in physiology · 2013Article
- The touching story of purinergic signaling in epithelial and endothelial cells.Purinergic signalling · 2012Review
- Basal release of ATP: an autocrine-paracrine mechanism for cell regulation.Science signaling · 2010Review
- ENaC, renal sodium excretion and extracellular ATP.Purinergic signalling · 2009Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Aldosterone, the most important sodium-retaining hormone, was first characterized >50 years ago. However, despite numerous studies including the classical work of Isidore S. "Izzy" Edelman showing that aldosterone action depended on ATP production, the mechanism by which it activates sodium reabsorption via the epithelial sodium channel remains unclear. Here, we report experiments that suggest that one of the key steps in aldosterone action is via an autocrine/paracrine system. The hormone stimulates ATP release from the basolateral side of the target kidney cell. Prevention of ATP accumulation or its removal blocks aldosterone action. ATP then acts via a purinergic mechanism to produce contraction of small groups of adjacent epithelial cells. Patch clamping demonstrates that it is these contracted cells that have channel activity. With progressive recruitment of contracting cells, there is then a parallel increase in transepithelial electrical conductance. In common with other stimuli of sodium transport, this pathway involves phosphatidylinositol 3-kinase. Inhibition of phosphatidylinositol 3-kinase blocks both cell contraction and conductance. We put forward the hypothesis that redistribution of the cell volume caused by the lateral contraction results in apical swelling and that this change, in turn, disrupts the epithelial sodium channel interaction with the F-actin cytoskeleton, opening the channel and hence increasing sodium transport.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.