title: Increase in Vascular Injury of Sodium Overloaded Mice May be Related to Vascular Angiotensin Modulation.
abstract: This study aimed to analyzing the effect of chronic sodium overload upon carotid and femoral injury, and its relation to vascular angiotensin modulation. Male C57Bl6 mice were divided in: control (cont), receiving 1% NaCl solution for 2 weeks (salt-2) or 12 weeks (salt-12). Two-weeks before the end of the study, a 2mm catheter was implanted around the left femoral and carotid arteries to induce injury. Blood pressure (BP) and heart rate (HR) were measured at the end of the study by tail plethysmography. Arteries were collected and prepared for histological analysis to determine arterial thickening and perivascular collagen deposition. Angiotensin II and Ang(1-7) were quantified in fresh arteries using the HPLC method. There were no differences in body weight, BP and HR. Intima/media ratio had a similar increase in both injured arteries of cont and salt-2 mice, but a more pronounced increase was observed in salt-12 mice (31.1±6%). On the other hand, sodium overload modified perivascular collagen deposition, increasing thick fibers (cont: 0.5%; salt-2: 3.4%; salt-12: 0.6%) and decreasing thin fibers (cont: 7.4%; salt-2: 0.5%; salt-12: 6.8%) in non-injured arteries. Injured arteries presented similar collagen fiber distribution. Angiotensin quantification showed increased Ang(1-7) in salt treated mice (salt-2: +72%; salt-12: +45%) with a concomitant decrease in Ang II (salt-2: -54%; salt-12: -60%). Vascular injury increased significantly Ang(1-7) in salt-12 mice (+80%), maintaining Ang II reduction similar to that of a non-injured artery. The lack of changes in BP and HR suggests that the structural changes observed may be due to non-hemodynamic mechanisms such as local renin-angiotensin system. Collagen evaluation suggests that sodium overload induces time-related changes in vascular remodeling. The increase of artery injury with concomitant increase in Ang(1-7) in 12-week treated mice shows a direct association between the duration of salt treatment and the magnitude of vascular injury.
authors.affiliation: Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil.
authors.forename: Cintia Taniguti
authors.initials: CT
authors.lastname: Lima
authors.affiliation: Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil.
authors.forename: Juliane Cristina de Souza
authors.initials: JC
authors.lastname: Silva
authors.affiliation: Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil.
authors.forename: Katia Aparecida da Silva
authors.initials: KA
authors.lastname: Viegas
authors.affiliation: Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil.
authors.forename: Thais Cristina de Souza
authors.initials: TC
authors.lastname: Oliveira
authors.affiliation: Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil.
authors.forename: Rariane Silva de
authors.initials: RS
authors.lastname: Lima
authors.affiliation: Hypertension Unit, Heart Institute, University of São Paulo Medical School, São Paulo, São Paulo, Brazil.
authors.forename: Leandro Ezequiel de
authors.initials: LE
authors.lastname: Souza
authors.affiliation: Nephrology Division, Department of Medicine, Federal University of São Paulo, São Paulo, São Paulo, Brazil.
authors.forename: Danielle
authors.initials: D
authors.lastname: Aragão
authors.affiliation: Nephrology Division, Department of Medicine, Federal University of São Paulo, São Paulo, São Paulo, Brazil.
authors.forename: Dulce Elena
authors.initials: DE
authors.lastname: Casarini
authors.affiliation: Hypertension Unit, Heart Institute, University of São Paulo Medical School, São Paulo, São Paulo, Brazil.
authors.forename: Maria Claudia
authors.initials: MC
authors.lastname: Irigoyen
authors.affiliation: Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil.
authors.forename: Silvia
authors.initials: S
authors.lastname: Lacchini
mesh_terms: D000809:Angiotensins / Q000378:metabolism*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002339:Carotid Arteries / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000502:physiology; D020212:Carotid Artery Injuries / Q000139:chemically induced*; D003094:Collagen / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004548:Elasticity; D005263:Femoral Artery / Q000187:drug effects* / Q000293:injuries* / Q000473:pathology / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D058426:Neointima / Q000139:chemically induced; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D012965:Sodium Chloride / Q000009:adverse effects*; D066253:Vascular Remodeling / Q000187:drug effects
chemical_list: D000809:Angiotensins; D012965:Sodium Chloride; D003094:Collagen; D007703:Peptidyl-Dipeptidase A