Regulation of vascular tone by cGMP and cAMP
Description
The binding of an agonist to M3 receptors carries out the formation of IP3 which triggers activation NOS that release NO, into the VSMC, NO generates cGMP, this binds to the protein kinase G, which prevente the entry of Ca2+. PKG also activates SERCA
AA is released from the phospholipids of the endothelial cell membrane, by the action of COX-1 generate PGI2, the binding of PGI2 to the IP recepto on VSMC triggers the conversion of cAMP, which binds to protein kinase A, favoring vasorelaxation
Acknowledgements
References
Vanhoutte, P. M., Zhao, Y., Xu, A., & Leung, S. W. (2016). Thirty years of saying NO: sources, fate, actions, and misfortunes of the endothelium-derived vasodilator mediator. Circulation research, 119(2), 375-396.
Baretella, O., & Vanhoutte, P. M. (2016). Endothelium-dependent contractions: prostacyclin and endothelin-1, partners in crime?. In Advances in Pharmacology (Vol. 77, pp. 177-208). Academic Press.
Cahill, P. A., & Redmond, E. M. (2016). Vascular endothelium–gatekeeper of vessel health. Atherosclerosis, 248, 97-109.
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