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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Increase in Vascular Injury of Sodium Overloaded Mice May be Related to Vascular Angiotensin Modulation

Texto completo
Autor(es):
Lima, Cintia Taniguti [1] ; de Souza Silva, Juliane Cristina [1] ; da Silva Viegas, Katia Aparecida [1] ; de Souza Oliveira, Thais Cristina [1] ; de Lima, Rariane Silva [1] ; de Souza, Leandro Ezequiel [2] ; Aragao, Danielle [3] ; Casarini, Dulce Elena [3] ; Irigoyen, Maria Claudia [2] ; Lacchini, Silvia [1]
Número total de Autores: 10
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Anat, Sao Paulo, SP - Brazil
[2] Univ Sao Paulo, Sch Med, Inst Heart, Hypertens Unit, Sao Paulo, SP - Brazil
[3] Univ Fed Sao Paulo, Dept Med, Div Nephrol, Sao Paulo, SP - Brazil
Número total de Afiliações: 3
Tipo de documento: Artigo Científico
Fonte: PLoS One; v. 10, n. 6 JUN 1 2015.
Citações Web of Science: 1
Resumo

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. (AU)

Processo FAPESP: 08/56192-7 - Efeito da sobrecarga salina sobre a resposta a injuria vascular em camundongos: possivel participacao do sistema renina-angiotensina
Beneficiário:Cintia Taniguti Lima
Modalidade de apoio: Bolsas no Brasil - Mestrado