ArticleThe Journal of physiology2006
The cellular mechanisms by which adenosine evokes release of nitric oxide from rat aortic endothelium.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 107 citations in OpenAlex.
- Renal Ischemia-Reperfusion and Uremic Toxins Modulate the Aortic Adenosinergic Axis in Acute Kidney Injury.International journal of molecular sciences · 2026Article
- Microvascular arteriolar reactivity in response to skeletal muscle contractions in female and male hamsters.Physiological reports · 2025Article
- CamKIIα and VPAC1 Expressions in the Caudal Trigeminal Nucleus of Rats After Systemic Nitroglycerin Treatment: Interaction with Anandamide.Life (Basel, Switzerland) · 2025Article
- Antihypertensive Effect of New Agonist of Adenosine Receptor in Spontaneously Hypertensive Rats.Arquivos brasileiros de cardiologia · 2024Article
- Migraine signaling pathways: purine metabolites that regulate migraine and predispose migraineurs to headache.Molecular and cellular biochemistry · 2023Review
- Ion Channel Disturbances in Migraine Headache: Exploring the Potential Role of the Kynurenine System in the Context of the Trigeminovascular System.International journal of molecular sciences · 2023Review
- Adenosine Receptors Profile in Fibromuscular Dysplasia.Biomedicines · 2022Article
- Review
- Adenosine, Adenosine Receptors and Neurohumoral Syncope: From Molecular Basis to Personalized Treatment.Biomedicines · 2022Review
- Targeting BKCNS drugs · 2020Review
- Adenosine and the Cardiovascular System.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2019Review
- G-Protein-Coupled Receptors in Heart Disease.Circulation research · 2018Review
- Characterization of the trigeminovascular actions of several adenosine AThe journal of headache and pain · 2018Article
- Increased ATP and ADO Overflow From Sympathetic Nerve Endings and Mesentery Endothelial Cells Plus Reduced Nitric Oxide Are Involved in Diabetic Neurovascular Dysfunction.Frontiers in pharmacology · 2018Article
- The KThe journal of headache and pain · 2017Article
- The Adenosinergic System as a Therapeutic Target in the Vasculature: New Ligands and Challenges.Molecules (Basel, Switzerland) · 2017Review
- Augmentation of Muscle Blood Flow by Ultrasound Cavitation Is Mediated by ATP and Purinergic Signaling.Circulation · 2017Article
- The Adenosine Hypothesis Revisited: Modulation of Coupling between Myocardial Perfusion and Arterial Compliance.Frontiers in physiology · 2017Article
- Adenosine Receptors As Drug Targets for Treatment of Pulmonary Arterial Hypertension.Frontiers in pharmacology · 2017Review
- Hypoxia and hyperoxia potentiate PAF receptor-mediated effects in newborn ovine pulmonary arterial smooth muscle cells: significance in oxygen therapy of PPHN.Physiological reports · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenosine and nitric oxide (NO) are important local mediators of vasodilatation. The aim of this study was to elucidate the mechanisms underlying adenosine receptor-mediated NO release from the endothelium. In studies on freshly excised rat aorta, second-messenger systems were pharmacologically modulated by appropriate antagonists while a NO-sensitive electrode was used to measure adenosine-evoked NO release from the endothelium. We showed that A1-mediated NO release requires extracellular Ca2+, phospholipase A2 (PLA2) and ATP-sensitive K+ (KATP) channel activation whereas A2A-mediated NO release requires extracellular Ca2+ and Ca2+-activated K+ (KCa) channels. Since our previous study showed that A1- and A2A-receptor-mediated NO release requires activation of adenylate cyclase (AC), we propose the following novel pathways. The K+ efflux resulting from A1-receptor-coupled KATP-channel activation facilitates Ca2+ influx which may cause some stimulation of endothelial NO synthase (eNOS). However, the increase in [Ca2+]i also stimulates PLA2 to liberate arachidonic acid and stimulate cyclooxygenase to generate prostacyclin (PGI2). PGI2 acts on its endothelial receptors to increase cAMP, so activating protein kinase A (PKA) to phosphorylate and activate eNOS resulting in NO release. By contrast, the K+ efflux resulting from A2A-coupled KCa channels facilitates Ca2+ influx, thereby activating eNOS and NO release. This process may be facilitated by phosphorylation of eNOS by PKA via the action of A2A-receptor-mediated stimulation of AC increasing cAMP. These pathways may be important in mediating vasodilatation during exercise and systemic hypoxia when adenosine acting in an endothelium- and NO-dependent manner has been shown to be important.
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Registered trials
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