ArticlePurinergic signalling2009
ATP as a mediator of macula densa cell signalling.
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 28 papers.
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Who cites it
28 citing papers in PubMed, 68 citations in OpenAlex.
- Claudin-3 is expressed at theFrontiers in physiology · 2026Article
- Renal TRPM3 Channels Regulate Blood Pressure via Tubuloglomerular Feedback and Plasma Volume Control.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Assessment, molecular mechanisms and therapeutic targets for renal functional reserve.Renal failure · 2025Review
- Purinergic Receptor Antagonists: A Complementary Treatment for Hypertension.Pharmaceuticals (Basel, Switzerland) · 2024Review
- [New concepts in the physiopathology of hypertension. Purinergic receptors].Archivos de cardiologia de Mexico · 2024Review
- The ATP-Releasing Maxi-Cl Channel: Its Identity, Molecular Partners and Physiological/Pathophysiological Implications.Life (Basel, Switzerland) · 2021Review
- Purinoceptors, renal microvascular function and hypertension.Physiological research · 2020Review
- Extracellular Nucleotides and P2 Receptors in Renal Function.Physiological reviews · 2020Review
- Exposure to Hyperchloremia Is Associated with Poor Early Recovery of Kidney Graft Function after Living-Donor Kidney Transplantation: A Propensity Score-Matching Analysis.Journal of clinical medicine · 2019Article
- "I don't get no respect": the role of chloride in acute kidney injury.American journal of physiology. Renal physiology · 2019Review
- A colorimetric ATP assay based on the use of a magnesium(II)-dependent DNAzyme.Mikrochimica acta · 2019Article
- CD39-adenosinergic axis in renal pathophysiology and therapeutics.Purinergic signalling · 2018Review
- The organic anion transporter SLCO2A1 constitutes the core component of the Maxi-Cl channel.The EMBO journal · 2017Article
- Acute In Vivo Analysis of ATP Release in Rat Kidneys in Response to Changes of Renal Perfusion Pressure.Journal of the American Heart Association · 2017Article
- 0.9% saline is neither normal nor physiological.Journal of Zhejiang University. Science. B · 2016Review
- The properties, functions, and pathophysiology of maxi-anion channels.Pflugers Archiv : European journal of physiology · 2016Review
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- Should chloride-rich crystalloids remain the mainstay of fluid resuscitation to prevent 'pre-renal' acute kidney injury?: con.Kidney international · 2014Article
- Effects of NKCC2 isoform regulation on NaCl transport in thick ascending limb and macula densa: a modeling study.American journal of physiology. Renal physiology · 2014Article
- Purinergic signalling in the kidney in health and disease.Purinergic signalling · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Within each nephro-vascular unit, the tubule returns to the vicinity of its own glomerulus. At this site, there are specialised tubular cells, the macula densa cells, which sense changes in tubular fluid composition and transmit information to the glomerular arterioles resulting in alterations in glomerular filtration rate and blood flow. Work over the last few years has characterised the mechanisms that lead to the detection of changes in luminal sodium chloride and osmolality by the macula densa cells. These cells are true "sensor cells" since intracellular ion concentrations and membrane potential reflect the level of luminal sodium chloride concentration. An unresolved question has been the nature of the signalling molecule(s) released by the macula densa cells. Currently, there is evidence that macula densa cells produce nitric oxide via neuronal nitric oxide synthase (nNOS) and prostaglandin E(2) (PGE(2)) through cyclooxygenase 2 (COX 2)-microsomal prostaglandin E synthase (mPGES). However, both of these signalling molecules play a role in modulating or regulating the macula-tubuloglomerular feedback system. Direct macula densa signalling appears to involve the release of ATP across the basolateral membrane through a maxi-anion channel in response to an increase in luminal sodium chloride concentration. ATP that is released by macula densa cells may directly activate P2 receptors on adjacent mesangial cells and afferent arteriolar smooth muscle cells, or the ATP may be converted to adenosine. However, the critical step in signalling would appear to be the regulated release of ATP across the basolateral membrane of macula densa cells.
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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.