ArticleAmerican journal of physiology. Renal physiology2012
Modulation of bladder function by luminal adenosine turnover and A1 receptor activation.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Biomechanical regulation of bladder injury and repair.Nature reviews. Urology · 2026Review
- Identification of cis-regulatory elements provides insights into tissue-specific gene regulation in the sheep genome.Nature communications · 2026Article
- Sensory Neurons, PIEZO Channels and PAC1 Receptors Regulate the Mechanosensitive Release of Soluble Ectonucleotidases in the Murine Urinary Bladder Lamina Propria.International journal of molecular sciences · 2023Article
- Urinary ATP Levels Are Controlled by Nucleotidases Released from the Urothelium in a Regulated Manner.Metabolites · 2022Article
- Selective reduction of neurotransmitter release by cAMP-dependent pathways in mouse detrusor.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- The Urothelium: Life in a Liquid Environment.Physiological reviews · 2020Review
- Urinary KScientific reports · 2019Article
- RAB27B requirement for stretch-induced exocytosis in bladder umbrella cells.American journal of physiology. Cell physiology · 2018Article
- Urothelial purine release during filling of murine and primate bladders.American journal of physiology. Renal physiology · 2016Article
- A1 Adenosine Receptor-Mediated Inhibition of Parasympathetic Neuromuscular Transmission in Human and Murine Urinary Bladder.The Journal of pharmacology and experimental therapeutics · 2016Article
- Increased urothelial paracellular transport promotes cystitis.American journal of physiology. Renal physiology · 2015Article
- Effect of botulinum toxin A on urothelial-release of ATP and expression of SNARE targets within the urothelium.Neurourology and urodynamics · 2015Article
- A1 adenosine receptor-stimulated exocytosis in bladder umbrella cells requires phosphorylation of ADAM17 Ser-811 and EGF receptor transactivation.Molecular biology of the cell · 2014Article
- Purinergic signalling in the urinary tract in health and disease.Purinergic signalling · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
Abstract
The bladder uroepithelium transmits information to the underlying nervous and musculature systems, is under constant cyclical strain, expresses all four adenosine receptors (A(1), A(2A), A(2B), and A(3)), and is a site of adenosine production. Although adenosine has a well-described protective effect in several organs, there is a lack of information about adenosine turnover in the uroepithelium or whether altering luminal adenosine concentrations impacts bladder function or overactivity. We observed that the concentration of extracellular adenosine at the mucosal surface of the uroepithelium was regulated by ecto-adenosine deaminase and by equilibrative nucleoside transporters, whereas adenosine kinase and equilibrative nucleoside transporters modulated serosal levels. We further observed that enriching endogenous adenosine by blocking its routes of metabolism or direct activation of mucosal A(1) receptors with 2-chloro-N(6)-cyclopentyladenosine (CCPA), a selective agonist, stimulated bladder activity by lowering the threshold pressure for voiding. Finally, CCPA did not quell bladder hyperactivity in animals with acute cyclophosphamide-induced cystitis but instead exacerbated their irritated bladder phenotype. In conclusion, we find that adenosine levels at both surfaces of the uroepithelium are modulated by turnover, that blocking these pathways or stimulating A(1) receptors directly at the luminal surface promotes bladder contractions, and that adenosine further stimulates voiding in animals with cyclophosphamide-induced cystitis.
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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.