ArticleBritish journal of pharmacology2003
Extracellular L-arginine is required for optimal NO synthesis by eNOS and iNOS in the rat mesenteric artery wall.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 39 citations in OpenAlex.
- Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026Review
- Whitening and Anti-Inflammatory Activities of Exosomes Derived fromMolecules (Basel, Switzerland) · 2025Article
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- Pathophysiology of Preeclampsia and L-Arginine/L-Citrulline Supplementation as a Potential Strategy to Improve Birth Outcomes.Advances in experimental medicine and biology · 2023Review
- Evaluation of oral citrulline administration as a mitigation strategy for fescue toxicosis in sheep.Translational animal science · 2020Article
- Functional status of microvascular vasomotion is impaired in spontaneously hypertensive rat.Scientific reports · 2017Article
- Loss of p53 in stromal fibroblasts promotes epithelial cell invasion through redox-mediated ICAM1 signal.Free radical biology & medicine · 2013Article
- Extracellular arginine rapidly dilates in vivo intestinal arteries and arterioles through a nitric oxide mechanism.Microcirculation (New York, N.Y. : 1994) · 2008Article
- Inhibition of nitric oxide synthase enhances contractile response of ventricular myocytes from streptozotocin-diabetic rats.Molecular and cellular biochemistry · 2007Article
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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
1. The formation of NO from endothelial nitric oxide synthase (eNOS) in rat superior mesenteric artery rings was dependent on extracellular L-arginine, and was optimal at a concentration of L-arginine close to the plasma level (carbachol-stimulated NO: control 15.7+/-0.9, L-arginine 100 micro M 22.8+/-1.3 nM). 2. Enhancement of NO output by L-arginine was stereospecific, required the cationic amino-acid transporter and was dependent on caveolin. 3. Induction of inducible nitric oxide synthase (iNOS) impaired the stimulated NO synthesis from eNOS (100 nM carbachol-stimulated NO: control 5.7+/-0.6, iNOS 0.3+/-0.3 nM). 4. The interaction between iNOS and eNOS was reversed by the superoxide scavenger MnTMPyP. Impairment of eNOS by iNOS was also prevented by L-arginine 100 micro M administered simultaneously with carbachol, but not by L-arginine administered during incubation with lipopolysaccharide. 5. These data provide functional evidence that supplementing L-arginine from the extracellular medium optimises the formation of NO from eNOS and suggests that the impairment of eNOS by iNOS is caused by excess formation of superoxide by NO synthase, which can be prevented by L-arginine. These results provide an explanation for the observations that extracellular L-arginine can enhance endothelium function only when the endothelium is impaired or when iNOS has been induced.
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