ArticleAmerican journal of physiology. Heart and circulatory physiology2006
COX-2 contributes to the maintenance of flow-induced dilation in arterioles of eNOS-knockout mice.
Article in American journal of physiology. Heart and circulatory physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 48 citations in OpenAlex.
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- Roles of Endothelial Motilin Receptor and Its Signal Transduction Pathway in Motilin-Induced Left Gastric Artery Relaxation in Dogs.Frontiers in physiology · 2021Article
- Physiological Consequences of Coronary Arteriolar Dysfunction and Its Influence on Cardiovascular Disease.Physiology (Bethesda, Md.) · 2018Review
- Sexually Dimorphic Regulation of EET Synthesis and Metabolism: Roles of Estrogen.Frontiers in pharmacology · 2018Article
- Accelerated atherosclerosis development in C57Bl6 mice by overexpressing AAV-mediated PCSK9 and partial carotid ligation.Laboratory investigation; a journal of technical methods and pathology · 2017Article
- Effects of chronic nitric oxide synthase inhibition on V'ONaunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Transition in the mechanism of flow-mediated dilation with aging and development of coronary artery disease.Basic research in cardiology · 2017Article
- Vasomotor Reaction to Cyclooxygenase-1-Mediated Prostacyclin Synthesis in Carotid Arteries from Two-Kidney-One-Clip Hypertensive Mice.PloS one · 2015Article
- The SIRT1 activator SRT1720 reverses vascular endothelial dysfunction, excessive superoxide production, and inflammation with aging in mice.American journal of physiology. Heart and circulatory physiology · 2014Article
- Vascular TRP channels: performing under pressure and going with the flow.Physiology (Bethesda, Md.) · 2014Review
- Acidosis prevents and alkalosis augments endothelium-dependent contractions in mouse arteries.Pflugers Archiv : European journal of physiology · 2014Article
- Role of caveolae in shear stress-mediated endothelium-dependent dilation in coronary arteries.Cardiovascular research · 2013Article
- Molecular mechanisms regulating the vascular prostacyclin pathways and their adaptation during pregnancy and in the newborn.Pharmacological reviews · 2012Review
- Role of reactive oxygen and nitrogen species in the vascular responses to inflammation.Free radical biology & medicine · 2012Review
- A novel vascular EET synthase: role of CYP2C7.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Article
- Role of shear stress and stretch in vascular mechanobiology.Journal of the Royal Society, Interface · 2011Review
- Roles of CYP2C29 and RXR gamma in vascular EET synthesis of female mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- Article
- Differential involvement of COX1 and COX2 in the vasculopathy associated with the alpha-galactosidase A-knockout mouse.American journal of physiology. Heart and circulatory physiology · 2009Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Our previous studies demonstrated that, in gracilis muscle arterioles of male mice deficient in the gene for endothelial nitric oxide synthase (eNOS), flow-induced dilation (FID) is mediated by endothelial PGs. Thus the present study aimed to identify the specific isoform of cyclooxygenase (COX) responsible for the compensatory mediation of FID in arterioles of eNOS-knockout (KO) mice. Experiments were conducted on gracilis muscle arterioles of male eNOS-KO and wild-type (WT) mice. Basal tone and magnitude of FID of arterioles were comparable in the two strains of mice. A role for COX isoforms in the mediation of the responses was assessed by use of valeryl salicylate (3 mM) and NS-398 (10 microM), inhibitors of COX-1 and COX-2, respectively. In eNOS-KO arterioles, valeryl salicylate or NS-398 alone inhibited FID (at maximal flow rate) by approximately 51% and approximately 58%, respectively. Administration of both inhibitors eliminated the dilation. In WT arterioles, inhibition of COX-2 did not significantly affect FID, whereas inhibition of COX-1 decreased the dilation by approximately 57%. The residual portion of the response was abolished by additional administration of Nomega-nitro-L-arginine methyl ester. Western blot analysis indicated a comparable content of COX-1 protein in arterioles of WT and eNOS-KO mice. COX-2 protein, which was not detectable in arterioles of WT mice, was strongly expressed in arterioles of eNOS-KO mice, together with an upregulation of COX-2 gene expression. Immunohistochemical staining confirmed the presence of COX-2 in the endothelium of eNOS-KO arterioles. In conclusion, COX-2-derived PGs are the mediators responsible for maintenance of FID in arterioles of eNOS-deficient mice.
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