ArticleThorax2003
Role of the endothelium and nitric oxide synthases in modulating superoxide formation induced by endotoxin and cytokines in porcine pulmonary arteries.
Article in Thorax, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 85 citations in OpenAlex.
- Therapeutic Potential of Hydrogen Sulfide in Reproductive System Disorders.Biomolecules · 2024Review
- Role of hydrogen sulfide in the male reproductive system.Frontiers in endocrinology · 2024Review
- Coronary Microvascular Dysfunction and Heart Failure with Preserved Ejection Fraction - implications for Chronic Inflammatory Mechanisms.Current cardiology reviews · 2022Review
- Clotting Dysfunction in Sepsis: A Role for ROS and Potential for Therapeutic Intervention.Antioxidants (Basel, Switzerland) · 2021Review
- Non-canonical chemical feedback self-limits nitric oxide-cyclic GMP signaling in health and disease.Scientific reports · 2020Article
- A fission yeast platform for heterologous expression of mammalian adenylyl cyclases and high throughput screening.Cellular signalling · 2019Article
- The Interaction between Trolox and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic Acid on Hypoxic Pulmonary Vasoconstriction in the Isolated Rabbit Lung.Iranian journal of medical sciences · 2017Article
- Decreases in manganese superoxide dismutase expression and activity contribute to oxidative stress in persistent pulmonary hypertension of the newborn.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Statins as a novel therapeutic strategy in acute lung injury.Pulmonary circulation · 2012Article
- Vein graft failure: current clinical practice and potential for gene therapeutics.Gene therapy · 2012Review
- Effects of early administration of a novel anticholinergic drug on acute respiratory distress syndrome induced by sepsis.Medical science monitor : international medical journal of experimental and clinical research · 2011Article
- Article
- Effect of hydrogen sulphide-donating sildenafil (ACS6) on erectile function and oxidative stress in rabbit isolated corpus cavernosum and in hypertensive rats.BJU international · 2009Article
- H2S-donating sildenafil (ACS6) inhibits superoxide formation and gp91phox expression in arterial endothelial cells: role of protein kinases A and G.British journal of pharmacology · 2008Article
- Superoxide from NADPH oxidase upregulates type 5 phosphodiesterase in human vascular smooth muscle cells: inhibition with iloprost and NONOate.British journal of pharmacology · 2008Article
- Exercise training improves peripheral chemoreflex function in heart failure rabbits.Journal of applied physiology (Bethesda, Md. : 1985) · 2008Article
- Higher urine nitric oxide is associated with improved outcomes in patients with acute lung injury.American journal of respiratory and critical care medicine · 2007Article
- Nitric oxide synthase inhibitors appear to improve wound healing in endotoxemic rats: An investigator-blinded, controlled, experimental study.Current therapeutic research, clinical and experimental · 2006Article
- Lipopolysaccharide-induced alterations in oxygen consumption and radical generation in endothelial cells.Molecular and cellular biochemistry · 2005Article
- Sildenafil citrate and sildenafil nitrate (NCX 911) are potent inhibitors of superoxide formation and gp91phox expression in porcine pulmonary artery endothelial cells.British journal of pharmacology · 2005Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe interactive roles of cytokines, endotoxins, superoxide (O(2)(*-) ) and nitric oxide (NO) in the pathogenesis of adult respiratory distress syndrome (ARDS) have not been fully elucidated. The effects of tumour necrosis factor-alpha (TNF-alpha), interleukin 1alpha (IL-1alpha), and lipopolysaccharide (LPS) and the role of NO and the endothelium in mediating O(2)(*-) formation were therefore investigated in intact porcine pulmonary arteries in vitro.
methodsIntrapulmonary artery (PA) segments were obtained from White Landrace pigs (25-35 kg) and incubated with LPS, IL-1alpha, and TNF-alpha and O(2)(*-) release was measured by the superoxide dismutase (SOD) inhibitable reduction of ferricytochrome c. The source of O(2)(*-) formation was determined using a number of enzyme inhibitors. The role of NO was explored using NO synthase (NOS) inhibitors and the distribution of NOS isoforms and peroxynitrite (ONOO(-), an index of NO-O(2)(*-) interactions) assessed by immunocytochemistry.
resultsLPS, IL-1alpha, and TNF-alpha promoted the formation of O(2)(*-) from PA compared with untreated controls in a time and dose dependent manner, an effect markedly enhanced by removal of the endothelium but completely inhibited by the NADPH oxidase inhibitor diphenylene iodonium chloride (DPI). L-NAME and the eNOS inhibitor N(5)-(1-iminoethyl)-ornithine (L-NIO) enhanced O(2)(*-) formation from PA (with endothelium) in response to IL-1alpha and TNF-alpha but had no effect on LPS mediated O(2)(*-) formation, whereas L-NAME and the iNOS inhibitor L-N(6)-(1-iminoethyl)-lysine-HCl (L-NIL) enhanced O(2)(*-) formation only in response to LPS.
conclusionsLPS, IL-1alpha, and TNF-alpha promote O(2)(*-) formation through an upregulation of NADPH oxidase activity which is augmented by removal of the endothelium, as well as the inhibition of eNOS (in the case of cytokines) and iNOS (in the case of LPS). The concomitant expression of NOS isoforms (and NO formation) with that of NADPH oxidase may therefore constitute a protective system designed to remove O(2)(*-) through the formation of ONOO(-). If this is so, the integrity of the endothelium may be axiomatic in the progression and severity of ARDS.
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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.