ArticleThe Journal of physiology2002
Interactions of adenosine, prostaglandins and nitric oxide in hypoxia-induced vasodilatation: in vivo and in vitro studies.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 148 citations in OpenAlex.
- β-Adrenergic receptors mediate sex differences in vasodilation but not sympathetic-mediated vasoconstriction during hypoxia.American journal of physiology. Heart and circulatory physiology · 2025Trial
- Effects of modest hyperoxia and oral vitamin C on exercise hyperaemia and reactive hyperaemia in healthy young men.European journal of applied physiology · 2015Trial
- Different Placebos, Different Mechanisms, Different Outcomes: Lessons for Clinical Trials.PloS one · 2015Trial
- Combined inhibition of nitric oxide and vasodilating prostaglandins abolishes forearm vasodilatation to systemic hypoxia in healthy humans.The Journal of physiology · 2011Trial
- Exercise intensity-dependent contribution of beta-adrenergic receptor-mediated vasodilatation in hypoxic humans.The Journal of physiology · 2008Trial
- Circulating ATP-induced vasodilatation overrides sympathetic vasoconstrictor activity in human skeletal muscle.The Journal of physiology · 2004Trial
- Failure of systemic hypoxia to blunt alpha-adrenergic vasoconstriction in the human forearm.The Journal of physiology · 2003Trial
- Intermittent Hypoxia Associated with Sleep Apnea Disrupts Microvascular Hemodynamics and Oxygen Delivery.Communications biology · 2026Article
- The Role of Hyperbaric Oxygen Therapy in Neuroregeneration and Neuroprotection: A Review.Cureus · 2024Review
- Migraine signaling pathways: purine metabolites that regulate migraine and predispose migraineurs to headache.Molecular and cellular biochemistry · 2023Review
- Hypoxia-induced signaling in the cardiovascular system: pathogenesis and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- The forearm vascular response to sympathetic activation is attenuated in female, but not male, participants following acute intermittent hypoxia.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- Could respiration-driven blood oxygen changes modulate neural activity?Pflugers Archiv : European journal of physiology · 2023Review
- Monocyte Adhesion Assays for Detecting Endothelial Cell Activation in Vascular Inflammation and Atherosclerosis.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Sympathetic neurovascular transduction following acute hypoxia.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2021Article
- Sex differences in the vascular response to sympathetic activation during acute hypoxaemia.Experimental physiology · 2021Article
- Spatial and temporal patterns of nitric oxide diffusion and degradation drive emergent cerebrovascular dynamics.PLoS computational biology · 2020Article
- Prostaglandin contribution to postexercise hyperemia is dependent on tissue oxygenation during rhythmic and isometric contractions.Physiological reports · 2020Article
- Detection and response to acute systemic hypoxia.BJA education · 2020Article
- Resuscitation After Hemorrhagic Shock in the Microcirculation: Targeting Optimal Oxygen Delivery in the Design of Artificial Blood Substitutes.Frontiers in medicine · 2020Review
6 more citing papers are in PubMed but not listed here.
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4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenosine, prostaglandins (PG) and nitric oxide (NO) have all been implicated in hypoxia-evoked vasodilatation. We investigated whether their actions are interdependent. In anaesthetised rats, the PG synthesis inhibitors diclofenac or indomethacin reduced muscle vasodilatation evoked by systemic hypoxia or adenosine, but not that evoked by iloprost, a stable analogue of prostacyclin (PGI(2)), or by an NO donor. After diclofenac, the A(1) receptor agonist CCPA evoked no vasodilatation: we previously showed that A(1), but not A(2A), receptors mediate the hypoxia-induced muscle vasodilatation. Further, in freshly excised rat aorta, adenosine evoked a release of NO, detected with an NO-sensitive electrode, that was abolished by NO synthesis inhibition, or endothelium removal, and reduced by ~50 % by the A(1) antagonist DPCPX, the remainder being attenuated by the A(2A) antagonist ZM241385. Diclofenac reduced adenosine-evoked NO release by ~50 % under control conditions, abolished that evoked in the presence of ZM241385, but did not affect that evoked in the presence of DPCPX. Adenosine-evoked NO release was also abolished by the adenyl cyclase inhibitor 2',5'-dideoxyadenosine, while dose-dependent NO release was evoked by iloprost. Finally, stimulation of A(1), but not A(2A), receptors caused a release of PGI(2) from rat aorta, assessed by radioimmunoassay of its stable metabolite, 6-keto PGF(1alpha), that was abolished by diclofenac. These results suggest that during systemic hypoxia, adenosine acts on endothelial A(1) receptors to increase PG synthesis, thereby generating cAMP, which increases the synthesis and release of NO and causes muscle vasodilatation. This pathway may be important in other situations involving these autocoids.
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