ArticleThe Journal of membrane biology2003
Common actions of adenosine receptor agonists in modulating human trabecular meshwork cell transport.
Article in The Journal of membrane biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 39 citations in OpenAlex.
- Mechanistic Effects of Baicalein on Aqueous Humor Drainage and Intraocular Pressure.International journal of molecular sciences · 2022Article
- Adenosine A3 receptor activated in HAnnals of translational medicine · 2021Article
- Effect and Mechanism of Phosphodiesterase Inhibitors on Trabecular Outflow.Korean journal of ophthalmology : KJO · 2019Article
- Article
- Comparative Study of the Effects of Trabecular Meshwork Outflow Drugs on the Permeability and Nitric Oxide Production in Trabecular Meshwork Cells.Korean journal of ophthalmology : KJO · 2017Article
- Ocular Purine Receptors as Drug Targets in the Eye.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2016Review
- Discovery of Molecular Therapeutics for Glaucoma: Challenges, Successes, and Promising Directions.Journal of medicinal chemistry · 2016Review
- Endogenous production of extracellular adenosine by trabecular meshwork cells: potential role in outflow regulation.Investigative ophthalmology & visual science · 2012Article
- Recent Patents on Emerging Therapeutics for the Treatment of Glaucoma, Age Related Macular Degeneration and Uveitis.Recent patents on biomedical engineering · 2012Article
- Mechanisms of ATP release by human trabecular meshwork cells, the enabling step in purinergic regulation of aqueous humor outflow.Journal of cellular physiology · 2012Article
- Cytoskeletal dependence of adenosine triphosphate release by human trabecular meshwork cells.Investigative ophthalmology & visual science · 2011Article
- Sustained elevation of extracellular ATP in aqueous humor from humans with primary chronic angle-closure glaucoma.Experimental eye research · 2011Article
- Novel ocular antihypertensive compounds in clinical trials.Clinical ophthalmology (Auckland, N.Z.) · 2011Article
- Nucleoside-derived antagonists to A3 adenosine receptors lower mouse intraocular pressure and act across species.Experimental eye research · 2010Article
- Electron probe X-ray microanalysis of intact pathway for human aqueous humor outflow.American journal of physiology. Cell physiology · 2008Article
- Barrier qualities of the mouse eye to topically applied drugs.Experimental eye research · 2007Article
- Cell-specific differential modulation of human trabecular meshwork cells by selective adenosine receptor agonists.Experimental eye research · 2007Article
- [Functional significance of adenosine receptors in the eye and their dysregulation in pseudoexfoliation syndrome].Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft · 2005Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
A(1) adenosine receptors (ARs) reduce, and A(2)ARs increase intraocular pressure, partly by differentially altering resistance to aqueous humor outflow. It is unknown whether the opposing effects of A(1)AR and A(2)AR agonists are mediated at different outflow-pathway cell targets or by opposing actions on a single cell target. We tested whether a major outflow-pathway cell, the trabecular meshwork (TM) cell might constitute the primary AR-agonist target and respond differentially to A(1), A(2A) and A(3)AR agonists. Receptor activation in human TM cells was identified by applying subtype-selective AR agonists: CPA and ADAC for A(1)ARs, CGS 21680 and DPMA for A(2A)ARs, and Cl-IB-MECA and IB-MECA for A(3)ARs. Stimulation of A(1), A(2A) and A(3)ARs elevated Ca(2+), measured with fura-2. Whole-cell patch clamping indicated that AR agonists activated ion channels non-uniformly, possibly reflecting variability in magnitude of agonist-triggered second-messenger responses. A(1), A(2A) and A(3)AR agonists all reduced volume, determined by calcein cell imaging. The endogenous source of adenosine delivery to the outflow pathway could be the TM cells since these cells were stimulated to release ATP by hypotonic perfusion. We conclude that: (1) TM cells express functional A(1), A(2A) and A(3)ARs; and (2) the reported differential effects of AR agonists on aqueous humor outflow are not mediated by differential actions on TM-cell Ca(2+) and volume, but likely by actions on separate cell targets.
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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.