title: Increased arterial load alters aortic structural and functional properties during embryogenesis.
abstract: As in the adult dorsal aorta, the embryonic dorsal aorta is an important determinant of cardiovascular function, and increased stiffness may have secondary effects on cardiac and microcirculatory development. We previously showed that acutely and chronically increased arterial load via vitelline artery ligation (VAL) increases systemic arterial stiffness. To test the hypothesis that local dorsal aortic stiffness also increases, we measured aortic pulse-wave velocity (PWV) and assessed the active and passive properties (stress and strain) of isolated aortic segments. PWV along the dorsal aorta increased acutely and chronically after VAL. Analysis of isolated aortic active properties suggests that load-exposed aortas experienced higher stress, but not strain, at similar intraluminal pressures. When smooth muscle tone was relaxed, strain decreased in VAL vessels, whereas stress became similar to control vessels. Immunohistochemical analysis revealed that although aortic smooth muscle alpha-actin content was similar between groups, more cell layers expressed smooth muscle alpha-actin, and myocyte cell shape was markedly rounder in VAL embryos. Additionally, aortic and perivascular collagen type I and III content significantly increased in load-exposed VAL vessels. Increased production of these proteins is consistent with the observed increase in aortic PWV and decreased strain in VAL passive aortic segments. Thus the embryonic dorsal aorta is sensitive to increased arterial load and adapts by altering its material properties via changes in collagen content.
authors.affiliation: Molecular Physiology and Biophysics, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77071, USA. lucitti@bcm.edu
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Lucitti
authors.forename: Richard
authors.initials: R
authors.lastname: Visconti
authors.forename: Jacqueline
authors.initials: J
authors.lastname: Novak
authors.forename: Bradley B
authors.initials: BB
authors.lastname: Keller
mesh_terms: D000199:Actins / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000166:cytology / Q000196:embryology* / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology*; D002642:Chick Embryo; D024042:Collagen Type I / Q000235:genetics / Q000378:metabolism; D024061:Collagen Type III / Q000235:genetics / Q000378:metabolism; D047108:Embryonic Development / Q000235:genetics / Q000502:physiology*; D005786:Gene Expression Regulation; D008026:Ligation; D008833:Microcirculation / Q000502:physiology; D032383:Myocytes, Cardiac / Q000166:cytology / Q000502:physiology; D012039:Regional Blood Flow / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D000199:Actins; D024042:Collagen Type I; D024061:Collagen Type III