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. 2015 Dec 1;67(5):361–366. doi: 10.1097/FJC.0000000000000348

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Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially.

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Mechanisms for synthesis and action of endothelium-derived relaxing factors in addition to vasodilator PGs and NO; several candidates could act as endothelium-dependent hyperpolarization (EDH) factor. PGs, NO, and EDH factor cause relaxations of underlying vascular smooth muscle through the mechanisms mediated by cyclic AMP (cAMP), cyclic GMP (cGMP), and hyperpolarization mediated by opening of Ca-activated K (K_Ca) channels. AMPKα1, α1-subunit of AMP-activated protein kinase; CaM, calmodulin; CaMKKβ, Ca²⁺/CaM-dependent protein kinase β; COX, cyclooxygenase; EETs, epoxyeicosatrienoic acids; eNOS, endothelial NO synthase; EOX, epoxygenase; HETEs, hydroxyeicosatetraenoic acids; H₂O₂, hydrogen peroxide; IP₃, inositol trisphosphate; LOX, lipoxygenase; LTs, leukotrienes; ONOO⁻, peroxynitrite; PKG_1α, 1α-subunit of protein kinase G; PLA2, phospholipase A2; PLC, phospholipase C.