MOLECULAR ASPECTS OF MEDICINE

dc.creatorSilva, Luis
dc.creatorSubiabre, Mario
dc.creatorAraos, Joaquin
dc.creatorSaez, Tamara
dc.creatorSalsoso, Rocio
dc.creatorPardo, Fabián
dc.creatorLeiva-Mendoza, Andrea Alejandra
dc.creatorSan Martin, Rody
dc.creatorToledo, Fernando
dc.creatorSobrevia, Luis
dc.date2021-08-23T23:00:19Z
dc.date2022-07-07T14:58:17Z
dc.date2021-08-23T23:00:19Z
dc.date2022-07-07T14:58:17Z
dc.date2017
dc.date.accessioned2023-08-22T22:59:54Z
dc.date.available2023-08-22T22:59:54Z
dc.identifier1150344
dc.identifier1150344
dc.identifierhttps://hdl.handle.net/10533/252823
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8349311
dc.descriptionRegulation of blood flow depends on systemic and local release of vasoactive molecules such as insulin and adenosine. These molecules cause vasodilation by activation of plasma membrane receptors at the vascular endothelium. Adenosine activates at least four subtypes of adenosine receptors (A(1)AR, A(2A)AR, A(2B)AR, A(3)AR), of which A(2A)AR and A(2B)AR activation leads to increased cAMP level, generation of nitric oxide, and relaxation of the underlying smooth muscle cell layer. Vasodilation caused by adenosine also depends on plasma membrane hyperpolarization due to either activation of intermediate-conductance Ca2+-activated K+ channels in vascular smooth muscle or activation of ATP-activated K+ channels in the endothelium. Adenosine also causes vasoconstriction via a mechanism involving A(1)AR activation resulting in lower cAMP level and increased thromboxane release. Insulin has also a dual effect causing NO-dependent vasodilation, but also sympathetic activity-and increased endothelin 1 release-dependent vasoconstriction. Interestingly, insulin effects require or are increased by activation or inactivation of adenosine receptors. This is phenomenon described for D-glucose and L-arginine transport where A(2A)AR and A(2B)AR play a major role. Other studies show that A(1)AR activation could reduce insulin release from pancreatic beta-cells. Whether adenosine modulation of insulin biological effect is a phenomenon that depends on co-localization of adenosine receptors and insulin receptors, and adenosine plasma membrane transporters is something still unclear. This review summarizes findings addressing potential involvement of adenosine receptors to modulate insulin effect via insulin receptors with emphasis in the human vasculature. (C) 2016 Elsevier Ltd. All rights reserved.
dc.descriptionRegular 2015
dc.descriptionFONDECYT
dc.descriptionFONDECYT
dc.languageeng
dc.relationhandle/10533/111557
dc.relationhandle/10533/111541
dc.relationhandle/10533/108045
dc.relationhttps://doi.org/10.1016/j.mam.2016.11.002
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 Chile
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.rightsinfo:eu-repo/semantics/article
dc.rightsinfo:eu-repo/semantics/openAccess
dc.titleInsulin/adenosine axis linked signalling
dc.titleMOLECULAR ASPECTS OF MEDICINE
dc.typeArticulo
dc.typeinfo:eu-repo/semantics/publishedVersion


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