ArticlePurinergic signalling2009
ENaC, renal sodium excretion and extracellular ATP.
Article in Purinergic signalling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
The trial behind it
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Hypothetical dysfunction of the epithelial sodium channel may justify neurohumoral blockade in coronavirus disease 2019.ESC heart failure · 2021Article
- Salt-deficient diet exacerbates cystogenesis in ARPKD via epithelial sodium channel (ENaC).EBioMedicine · 2019Article
- Genetic Deletion of P2YFrontiers in physiology · 2018Article
- P2X Receptors Inhibit NaCl Absorption in mTAL Independently of Nitric Oxide.Frontiers in physiology · 2017Article
- Functional and therapeutic importance of purinergic signaling in polycystic kidney disease.American journal of physiology. Renal physiology · 2016Review
- Clopidogrel attenuates lithium-induced alterations in renal water and sodium channels/transporters in mice.Purinergic signalling · 2015Article
- The Polarized Effect of Intracellular Calcium on the Renal Epithelial Sodium Channel Occurs as a Result of Subcellular Calcium Signaling Domains Maintained by Mitochondria.The Journal of biological chemistry · 2015Article
- P2X4 receptor regulation of transient receptor potential melastatin type 6 (TRPM6) Mg2+ channels.Pflugers Archiv : European journal of physiology · 2014Article
- Basolateral P2X₄channels stimulate ENaC activity in Xenopus cortical collecting duct A6 cells.American journal of physiology. Renal physiology · 2014Article
- Purinergic signalling in the kidney in health and disease.Purinergic signalling · 2014Review
- Introduction and perspective, historical note.Frontiers in cellular neuroscience · 2013Review
- Afferent Arteriolar Responses to β,γ-methylene ATP and 20-HETE are not Blocked by ENaC Inhibition.Physiological reports · 2013Article
- Sympathetic nerve-derived ATP regulates renal medullary vasa recta diameter via pericyte cells: a role for regulating medullary blood flow?Frontiers in physiology · 2013Article
- Defective renal water handling in transgenic mice over-expressing human CD39/NTPDase1.American journal of physiology. Renal physiology · 2012Article
- P2Y receptors and kidney function.Wiley interdisciplinary reviews. Membrane transport and signaling · 2012Article
- Role of BK channels in hypertension and potassium secretion.Current opinion in nephrology and hypertension · 2011Review
- P2Y₂ receptor activation decreases blood pressure and increases renal Na⁺ excretion.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Article
- Renal sodium transporter/channel expression and sodium excretion in P2Y2 receptor knockout mice fed a high-NaCl diet with/without aldosterone infusion.American journal of physiology. Renal physiology · 2011Article
- Effects of extracellular nucleotides on renal tubular solute transport.Purinergic signalling · 2009Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sodium balance determines the extracellular fluid volume and sets arterial blood pressure (BP). Chronically raised BP (hypertension) represents a major health risk in Western societies. The relationship between BP and renal sodium excretion (the pressure/natriuresis relationship) represents the key element in defining the BP homeostatic set point. The renin-angiotensin-aldosterone system (RAAS) makes major adjustments to the rates of renal sodium secretion, but this system works slowly over a period of hours to days. More rapid adjustments can be made by the sympathetic nervous system, although the kidney can function well without sympathetic nerves. Attention has now focussed on regulatory mechanisms within the kidney, including extracellular nucleotides and the P2 receptor system. Here, we discuss how extracellular ATP can control renal sodium excretion by altering the activity of epithelial sodium channels (ENaC) present in the apical membrane of principal cells. There remains considerable controversy over the molecular targets for released ATP, although the P2Y(2) receptor has received much attention. We review the available data and reflect on our own findings in which ATP-activated P2Y and P2X receptors make adjustments to ENaC activity and therefore sodium excretion.
Identifiers
What OpenQuestion holds
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.