Endothelium-Dependent Vasodilation: Nitric Oxide and Other Mediators
| Autor: | Denise C. Fernandes, Paulo Ferreira Leite, Francisco R.M. Laurindo, Marcel Liberman |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Endothelium Superoxide Vasodilation 030204 cardiovascular system & hematology Cyclase Nitric oxide Endothelial stem cell 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology 0302 clinical medicine Mediator medicine.anatomical_structure chemistry Biophysics medicine Peroxynitrite |
| DOI: | 10.1016/b978-0-12-812348-5.00008-8 |
| Popis: | Vasodilation is the archetypal function of the endothelial cell and the discovery of paracrine-dependent vasorelaxation by endothelium-derived production of the gaseous mediator nitric oxide (NO) was revolutionary. NO mediates its regulatory vasorelaxing effects through guanilyl cyclase activation. Also, thiol S-nitrosation by NO is increasingly evident as an effector mechanism. Another important NO-related chemistry is its reaction with superoxide radicals, yielding peroxynitrite and related oxidant and nitrating species associated with toxic effects. Nitrogen oxides are storage forms of NO which can exert vasodilation in the presence of hemeproteins. NO generation is mediated by NO synthase enzymes (endothelial, neuronal, and inducible isoforms), which depict complex regulation dependent on cofactors. The absence of such cofactors can uncouple NO generation from electron transfer, generating superoxide. The endothelium additional promotes vasodilation, mainly of small resistance arteries, through endothelium-derived hyperpolarizing factor(s) such as hydrogen peroxide, epoximetabolites of arachidonic acid, and gap junctions. Hydrogen sulfide is a novel gaseous endothelium-derived vasodilator. Together, these mechanisms compose an integrative platform providing an endothelium-associated dilator tone. |
| Databáze: | OpenAIRE |
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