title: Mechanisms of the inward remodeling process in resistance vessels: is the actin cytoskeleton involved?
abstract: The resistance arteries and arterioles are the vascular components of the circulatory system where the greatest drop in blood pressure takes place. Consequently, these vessels play a preponderant role in the regulation of blood flow and the modulation of blood pressure. For this reason, the inward remodeling process of the resistance vasculature, as it occurs in hypertension, has profound consequences on the incidence of life-threatening cardiovascular events. In this manuscript, we review some of the most prominent characteristics of inwardly remodeled resistance arteries including their changes in vascular passive diameter, wall thickness, and elastic properties. Then, we explore the known contribution of the different components of the vascular wall to the characteristics of inwardly remodeled vessels, and pay particular attention to the role the vascular smooth muscle actin cytoskeleton may play on the initial stages of the remodeling process. We end by proposing potential ways by which many of the factors and mechanisms known to participate in the inward remodeling process may be associated with cytoskeletal modifications and participate in reducing the passive diameter of resistance vessels.
authors.affiliation: Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, USA; Department of Biological Engineering, University of Missouri, Columbia, Missouri, USA.
authors.forename: Jorge A
authors.initials: JA
authors.lastname: Castorena-Gonzalez
authors.forename: Marius C
authors.initials: MC
authors.lastname: Staiculescu
authors.forename: Christopher
authors.initials: C
authors.lastname: Foote
authors.forename: Luis A
authors.initials: LA
authors.lastname: Martinez-Lemus
mesh_terms: D008841:Actin Cytoskeleton / Q000502:physiology*; D000818:Animals; D001158:Arteries / Q000033:anatomy & histology / Q000502:physiology; D001696:Biomechanical Phenomena; D055119:Elastic Modulus; D019204:GTP-Binding Proteins / Q000378:metabolism; D006801:Humans; D020782:Matrix Metalloproteinases / Q000378:metabolism; D008833:Microcirculation / Q000502:physiology; D055806:Microvessels / Q000502:physiology; D008955:Models, Cardiovascular; D032389:Myocytes, Smooth Muscle / Q000502:physiology; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases / Q000378:metabolism; D066253:Vascular Remodeling / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology; D020744:rac GTP-Binding Proteins / Q000378:metabolism; D020741:rho GTP-Binding Proteins / Q000378:metabolism
chemical_list: D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases; D020782:Matrix Metalloproteinases; D019204:GTP-Binding Proteins; D020744:rac GTP-Binding Proteins; D020741:rho GTP-Binding Proteins
keywords: Rac; Rho; actin polymerization; elasticity; hypertension; matrix metalloproteinases; stiffness; strain; stress; transglutaminase