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dc.contributor.authorCiocanel, Maria-Veronica
dc.contributor.authorStepien, Tracy
dc.contributor.authorSgouralis, Ioannis
dc.contributor.authorLayton, Anita
dc.date.accessioned2018-12-05T23:16:55Z
dc.date.available2018-12-05T23:16:55Z
dc.date.issued2018-07
dc.identifier.citationCiocanel M-V, Stepien TL, Sgouralis I, Layton AT. A Multicellular Vascular Model of the Renal Myogenic Response. Processes. 2018; 6(7):89.en_US
dc.identifier.issn2227-9717
dc.identifier.doi10.3390/pr6070089
dc.identifier.urihttp://hdl.handle.net/10150/631125
dc.description.abstractThe myogenic response is a key autoregulatory mechanism in the mammalian kidney. Triggered by blood pressure perturbations, it is well established that the myogenic response is initiated in the renal afferent arteriole and mediated by alterations in muscle tone and vascular diameter that counterbalance hemodynamic perturbations. The entire process involves several subcellular, cellular, and vascular mechanisms whose interactions remain poorly understood. Here, we model and investigate the myogenic response of a multicellular segment of an afferent arteriole. Extending existing work, we focus on providing an accurate-but still computationally tractable-representation of the coupling among the involved levels. For individual muscle cells, we include detailed Ca2+ signaling, transmembrane transport of ions, kinetics of myosin light chain phosphorylation, and contraction mechanics. Intercellular interactions are mediated by gap junctions between muscle or endothelial cells. Additional interactions are mediated by hemodynamics. Simulations of time-independent pressure changes reveal regular vasoresponses throughout the model segment and stabilization of a physiological range of blood pressures (80-180 mmHg) in agreement with other modeling and experimental studies that assess steady autoregulation. Simulations of time-dependent perturbations reveal irregular vasoresponses and complex dynamics that may contribute to the complexity of dynamic autoregulation observed in vivo. The ability of the developed model to represent the myogenic response in a multiscale and realistic fashion, under feasible computational load, suggests that it can be incorporated as a key component into larger models of integrated renal hemodynamic regulation.en_US
dc.description.sponsorshipNSF Award [DBI-1300426]; National Institutes of Health: National Institute of Diabetes and Digestive and Kidney Diseases grant [DK089066]; National Science Foundation [DMS-1263995]en_US
dc.language.isoenen_US
dc.publisherMDPIen_US
dc.relation.urlhttp://www.mdpi.com/2227-9717/6/7/89en_US
dc.rights© 2018 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.en_US
dc.subjectnonlinear modelen_US
dc.subjectsmooth muscleen_US
dc.subjectgap junctionsen_US
dc.subjectmicrocirculationen_US
dc.subjectkidneyen_US
dc.subjecthemodynamicsen_US
dc.titleA Multicellular Vascular Model of the Renal Myogenic Responseen_US
dc.typeArticleen_US
dc.contributor.departmentUniv Arizona, Dept Mathen_US
dc.identifier.journalPROCESSESen_US
dc.description.noteOpen access journal.en_US
dc.description.collectioninformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.en_US
dc.eprint.versionFinal published versionen_US
dc.source.journaltitleProcesses
dc.source.volume6
dc.source.issue7
dc.source.beginpage89
refterms.dateFOA2018-12-05T23:16:56Z


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