ArticleScientific reports2017
Compensatory Vasodilator Mechanisms in the Ophthalmic Artery of Endothelial Nitric Oxide Synthase Gene Knockout Mice.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
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- Studies on the Effects of Hypercholesterolemia on Mouse Ophthalmic Artery Reactivity.Diseases (Basel, Switzerland) · 2023Article
- Effects of Resveratrol on Vascular Function in Retinal Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2023Article
- Article
- Ventilatory responses during and following hypercapnic gas challenge are impaired in male but not female endothelial NOS knock-out mice.Scientific reports · 2021Article
- Short-term facilitation of breathing upon cessation of hypoxic challenge is impaired in male but not female endothelial NOS knock-out mice.Scientific reports · 2021Article
- Angiotensin II Induces Oxidative Stress and Endothelial Dysfunction in Mouse Ophthalmic Arteries via Involvement of AT1 Receptors and NOX2.Antioxidants (Basel, Switzerland) · 2021Article
- Arginase inhibition by (-)-Epicatechin reverses endothelial cell aging.European journal of pharmacology · 2020Article
- Bioenergetic shift and actin cytoskeleton remodelling as acute vascular adaptive mechanisms to angiotensin II in murine retina and ophthalmic artery.Redox biology · 2020Article
- Vasorelaxation elicited by endogenous and exogenous hydrogen sulfide in mouse mesenteric arteries.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- L-Arginine Ameliorates High-Fat Diet-Induced Atherosclerosis by Downregulating miR-221.BioMed research international · 2020Article
- Advanced Glycation End Products (AGEs) May Be a Striking Link Between Modern Diet and Health.Biomolecules · 2019Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) generated by endothelial nitric oxide synthase (eNOS) plays an important role in the maintenance of ocular vascular homeostasis. Therefore, perturbations in vascular NO synthesis have been implicated in the pathogenesis of several ocular diseases. We recently reported that eNOS contributes significantly to vasodilation of the mouse ophthalmic artery. Interestingly, dilatory responses were also retained in eNOS gene-deficient mice (eNOS-/-), indicating inherent endothelial adaptive mechanism(s) that act as back-up systems in chronic absence of eNOS to preserve vasorelaxation. Thus, this study endeavoured to identify the compensatory mechanism(s) in the ophthalmic artery of eNOS-/- mice employing isolated arterial segments and pharmacological inhibitors in vitro. Endothelium removal virtually abolished acetylcholine (ACh)-induced vasodilation, suggesting an obligatory involvement of the endothelium in cholinergic control of vascular tone. However, non-NOS and non-cyclooxygenase components compensate for eNOS deficiency via endothelium-derived hyperpolarizing factors (EDHFs). Notably, arachidonic acid-derived metabolites of the 12-lipoxygenase pathway were key mediators in activating the inwardly rectifying potassium channels to compensate for chronic lack of eNOS. Conclusively, endothelium-dependent cholinergic responses of the ophthalmic artery in the eNOS-/- mice are largely preserved and, this vascular bed has the ability to compensate for the loss of normal vasodilator responses solely via EDHFs.
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