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. 2022 Mar 19;11(6):1047. doi: 10.3390/cells11061047

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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The vasodilation–vasoconstriction competition hypothesis. (A) Schematic illustration of the main players involved in NO and 20-HETE release, according to [21]. Vasodilation is mediated by the NMDAR-NOS-NO pathway, while vasoconstriction is mediated by the mGluR-PLA-20-HETE pathway. Notice that NO inhibits 20-HETE synthesis [8]. PLA, phospholipase A; GC, guanylyl cyclase; PDE, phosphodiesterase. (B) Schematic illustration of the competition between NO and 20-HETE in determining vessel diameter changes. [NO] (red) is directly proportional to the simulated NMDA current (not shown), while capillary dilation (violet) is provided by experimental measurements (the difference between the two curves is in yellow). The 20-HETE is specular to the NVC inflection at intermediate frequencies (more details are given in text). (C) The differential engagement on the NO and 20-HETE pathways are shown for low, intermediate, and high stimulus frequencies (note the different thickness of the arrows).