ArticleCirculation research2009
Dual pathways of carbon monoxide-mediated vasoregulation: modulation by redox mechanisms.
Article in Circulation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
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Who cites it
17 citing papers in PubMed, 51 citations in OpenAlex.
- Carbon Monoxide Signaling: Examining Its Engagement with Various Molecular Targets in the Context of Binding Affinity, Concentration, and Biologic Response.Pharmacological reviews · 2022Review
- Carbon monoxide signaling and soluble guanylyl cyclase: Facts, myths, and intriguing possibilities.Biochemical pharmacology · 2022Review
- Carbon monoxide activation of delayed rectifier potassium currents of human cardiac fibroblasts through diverse pathways.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Carbon monoxide: An emerging therapy for acute kidney injury.Medicinal research reviews · 2020Review
- Targeting Heme Oxygenase-1 in Cardiovascular and Kidney Disease.Antioxidants (Basel, Switzerland) · 2019Review
- Characterization of a cellular denitrase activity that reverses nitration of cyclooxygenase.American journal of physiology. Heart and circulatory physiology · 2013Article
- Mechanisms of the vasorelaxing effects of CORM-3, a water-soluble carbon monoxide-releasing molecule: interactions with eNOS.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
- Antioxidants condition pleiotropic vascular responses to exogenous H(2)O(2): role of modulation of vascular TP receptors and the heme oxygenase system.Antioxidants & redox signaling · 2013Article
- Role of carbon monoxide in kidney function: is a little carbon monoxide good for the kidney?Current pharmaceutical biotechnology · 2012Review
- Carbon monoxide, generated by heme oxygenase-1, mediates the enhanced permeability and retention effect in solid tumors.Cancer science · 2012Article
- Regulation of ROS production and vascular function by carbon monoxide.Oxidative medicine and cellular longevity · 2012Review
- Enhanced hemeoxygenase activity in the rostral ventrolateral medulla mediates exaggerated hemin-evoked hypotension in the spontaneously hypertensive rat.The Journal of pharmacology and experimental therapeutics · 2011Article
- Carbon monoxide as an endogenous vascular modulator.American journal of physiology. Heart and circulatory physiology · 2011Review
- Immunohistochemical expression of fibronectin and C5b-9 in the myocardium in cases of carbon monoxide poisoning.International journal of legal medicine · 2011Article
- Redox regulation of guanylate cyclase and protein kinase G in vascular responses to hypoxia.Respiratory physiology & neurobiology · 2010Review
- Exhaled carbon monoxide and risk of metabolic syndrome and cardiovascular disease in the community.Circulation · 2010Article
- Effects of lactate and carbon monoxide interactions on neuroprotection and neuropreservation.Medical gas researchArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
rationaleVascular tissues produce carbon monoxide (CO) via HO-dependent and HO-independent mechanisms; the former in tandem with biliverdin and iron and the latter as a lone product. CO has been shown to function as both a vasoconstrictor and vasodilator; however, factors that dictate the vasoregulatory phenotype of this gas are unknown.
objectiveWe investigated whether CO-mediated vasoconstriction is mechanistically linked to enhanced reactive oxygen species production that masks vasodilatory pathways. METHODS AND
resultsSprague-Dawley rat interlobar and interlobular arteries were examined in terms of superoxide (O2*-) generation and vascular reactivity in the absence and presence of antioxidants. Both authentic CO and the CO-releasing molecule (CORM)-3 constricted renal arteries and increased O2*- production in a dose-dependent manner. The antioxidants tempol, ebselen, and deferoxamine inhibited CO-induced O2*- production and converted CO from constrictor to dilator. CO-induced O2*- generation was found to involve the activity of multiple oxidases including nitric oxide synthase, NADPH oxidase, xanthine oxidase, and complex IV of the mitochondrial electron chain. Furthermore, inhibition of these enzymes converted CO from constrictor to dilator. Similarly, biliverdin and bilirubin inhibited CO-induced O2*- production and vasoconstriction, allowing for a vasodilatory response to CO to be expressed. CO-induced vasoconstriction was dependent on a non-thromboxane agonist of the thromboxane receptor, whereas vasodilatory mechanisms of CO relied on the activation of soluble guanylate cyclase and calcium-gated potassium channels.
conclusionsCO-induced vasoconstriction involves the generation of reactive oxygen species, which, when negated, allows for the expression of vasodilatory pathways which are masked by the primary oxidative stress response to this gas.
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Registered trials
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