ArticleBritish journal of pharmacology1999
Adenosine mediates relaxation of human small resistance-like coronary arteries via A2B receptors.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 77 citations in OpenAlex.
- Endothelial dysfunction in chronic kidney disease: a clinical perspective.American journal of physiology. Heart and circulatory physiology · 2025Review
- Adenosine AMolecular and cellular biochemistry · 2021Article
- Adenosine and adenosine receptor-mediated action in coronary microcirculation.Basic research in cardiology · 2021Review
- Pharmacological Insights Into Safety and Efficacy Determinants for the Development of Adenosine Receptor Biased Agonists in the Treatment of Heart Failure.Frontiers in pharmacology · 2021Article
- Adenosine and the Cardiovascular System.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2019Review
- Regulation of Coronary Blood Flow.Comprehensive Physiology · 2017Review
- The Role of Adenosine ABioMed research international · 2017Review
- Lidocaine relaxation in isolated rat aortic rings is enhanced by endothelial removal: possible role of KBMC anesthesiology · 2016Article
- Adenosine relaxation in isolated rat aortic rings and possible roles of smooth muscle Kv channels, KATP channels and A2a receptors.BMC pharmacology & toxicology · 2016Article
- The Human Microcirculation: Regulation of Flow and Beyond.Circulation research · 2016Review
- Cardiac purinergic signalling in health and disease.Purinergic signalling · 2015Review
- Simulation and comparative analysis of binding modes of nucleoside and non-nucleoside agonists at the A2B adenosine receptor.In silico pharmacology · 2013Article
- CYP-epoxygenases contribute to A2A receptor-mediated aortic relaxation via sarcolemmal KATP channels.American journal of physiology. Regulatory, integrative and comparative physiology · 2012Article
- Contributions of A2A and A2B adenosine receptors in coronary flow responses in relation to the KATP channel using A2B and A2A/2B double-knockout mice.American journal of physiology. Heart and circulatory physiology · 2011Article
- Mechanisms involved in the adenosine-induced vasorelaxation to the pig prostatic small arteries.Purinergic signalling · 2011Article
- Adenosine receptor regulation of coronary blood flow in Ossabaw miniature swine.The Journal of pharmacology and experimental therapeutics · 2010Article
- Contribution of adenosine A(2A) and A(2B) receptors to ischemic coronary dilation: role of K(V) and K(ATP) channels.Microcirculation (New York, N.Y. : 1994) · 2010Article
- Altered mechanism of adenosine-induced coronary arteriolar dilation in early-stage metabolic syndrome.Experimental biology and medicine (Maywood, N.J.) · 2009Article
- Recent improvements in the development of A(2B) adenosine receptor agonists.Purinergic signalling · 2009Article
- Adenosine receptors and the heart: role in regulation of coronary blood flow and cardiac electrophysiology.Handbook of experimental pharmacology · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The receptor subtype and mechanisms underlying relaxation to adenosine were examined in human isolated small coronary arteries contracted with the thromboxane A2 mimetic, 1,5,5-hydroxy-11alpha, 9alpha-(epoxymethano)prosta-5Z, 13E-dienoic acid (U46619) to approximately 50% of their maximum contraction to K+ (125 mM) depolarization (Fmax). Relaxations were normalized as percentages of the 50% Fmax contraction. 2. Adenosine caused concentration-dependent relaxations (pEC50, 5.95+/-0.20; maximum relaxation (Rmax), 96.7+/-1.4%) that were unaffected by either combined treatment with the nitric oxide inhibitors, NG-nitro-L-arginine (L-NOARG; 100 microM) and oxyhaemoglobin (HbO; 20 microM) or the ATP-dependent K+ channel (KATP) inhibitor, glibenclamide (10 microM). The pEC50 but not Rmax to adenosine was significantly reduced by high extracellular K+ (30 mM). Relaxations to the adenylate cyclase activator, forskolin, however, were unaffected by high K+ (30 mM). 3. Adenosine and a range of adenosine analogues, adenosine, 2-chloroadenosine (2-CADO), 5'-N-ethyl-carboxamidoadenosine (NECA), R(-)-N6-(2-phenylisopropyl)-adenosine (R-PIA), S(+)-N6-(2-phenylisopropyl)-adenosine (S-PIA), N6-cyclopentyladenosine (CPA), 1-deoxy-1-[6-[[(3-iodophenyl)methyl]amino]-9H-purin-9-yl]-N-methyl-beta- D-ribofuranuronamide (IB-MECA), 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamido adenosine hydrochloride (CGS 21680), relaxed arteries with a rank order of potency of NECA= 2-CADO >adenosine= IB-MECA = R-PIA= CPA > S-PIA)> CGS 21680. 4. Sensitivity but not Rmax to adenosine was significantly reduced approximately 80 and 20 fold by the non-selective adenosine receptor antagonist, 8-(p-sulphophenyl)theophylline (8-SPT) and the A2 receptor antagonist, 3,7-dimethyl-1-propargylxanthine (DMPX). By contrast, the A1-selective antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) had no effect on pEC50 or Rmax to adenosine. 5. These results suggest that A2B receptors mediate relaxation to adenosine in human small coronary arteries which is independent of NO but dependent in part on a K+-sensitive mechanism.
Indexed as
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.