Cargando…

Time-Related Alteration in Flow- (Shear Stress-) Mediated Remodeling in Resistance Arteries from Spontaneously Hypertensive Rats

Hypertension is a major risk factor for cardiovascular disorders. As flow-mediated outward remodeling has a key role in postischemic revascularization, we investigated this remodeling in mesenteric resistance arteries of normotensive (WKY) and spontaneously hypertensive rats (SHRs) aged 3 to 9 month...

Descripción completa

Detalles Bibliográficos
Autores principales: Dumont, Odile, Kauffenstein, Gilles, Guihot, Anne-Laure, Guérineau, Nathalie C., Abraham, Pierre, Loufrani, Laurent, Henrion, Daniel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4034663/
https://www.ncbi.nlm.nih.gov/pubmed/24900916
http://dx.doi.org/10.1155/2014/859793
_version_ 1782318000147267584
author Dumont, Odile
Kauffenstein, Gilles
Guihot, Anne-Laure
Guérineau, Nathalie C.
Abraham, Pierre
Loufrani, Laurent
Henrion, Daniel
author_facet Dumont, Odile
Kauffenstein, Gilles
Guihot, Anne-Laure
Guérineau, Nathalie C.
Abraham, Pierre
Loufrani, Laurent
Henrion, Daniel
author_sort Dumont, Odile
collection PubMed
description Hypertension is a major risk factor for cardiovascular disorders. As flow-mediated outward remodeling has a key role in postischemic revascularization, we investigated this remodeling in mesenteric resistance arteries of normotensive (WKY) and spontaneously hypertensive rats (SHRs) aged 3 to 9 months. Sequential ligation of mesenteric resistance arteries allowed modifying blood flow in vivo, thus exposing arteries to low, normal, or high flow. After 1, 3, 8, or 24 weeks, arteries were isolated for in vitro study. High flow (HF) induced outward hypertrophic remodeling in WKY rats after 1 week and persisted until 24 weeks without change in wall to lumen ratio. In SHRs, diameter increase was delayed, occurring only after 3 weeks. Nevertheless, it was reduced at 8 weeks and no longer significant after 24 weeks. In parallel, media cross-section area increased more with time in SHRs than in WKY rats and this was associated with increased contractility and oxidative stress with decreased NO-dependent relaxation. Low flow induced progressive inward remodeling until 24 weeks in both strains with excessive hypertrophy in SHRs. Thus, a chronic increase in flow induced transitory diameter expansion and long-lasting hypertrophy in SHRs. This could contribute to the higher susceptibility of hypertensive subjects to ischemic diseases.
format Online
Article
Text
id pubmed-4034663
institution National Center for Biotechnology Information
language English
publishDate 2014
publisher Hindawi Publishing Corporation
record_format MEDLINE/PubMed
spelling pubmed-40346632014-06-04 Time-Related Alteration in Flow- (Shear Stress-) Mediated Remodeling in Resistance Arteries from Spontaneously Hypertensive Rats Dumont, Odile Kauffenstein, Gilles Guihot, Anne-Laure Guérineau, Nathalie C. Abraham, Pierre Loufrani, Laurent Henrion, Daniel Int J Hypertens Research Article Hypertension is a major risk factor for cardiovascular disorders. As flow-mediated outward remodeling has a key role in postischemic revascularization, we investigated this remodeling in mesenteric resistance arteries of normotensive (WKY) and spontaneously hypertensive rats (SHRs) aged 3 to 9 months. Sequential ligation of mesenteric resistance arteries allowed modifying blood flow in vivo, thus exposing arteries to low, normal, or high flow. After 1, 3, 8, or 24 weeks, arteries were isolated for in vitro study. High flow (HF) induced outward hypertrophic remodeling in WKY rats after 1 week and persisted until 24 weeks without change in wall to lumen ratio. In SHRs, diameter increase was delayed, occurring only after 3 weeks. Nevertheless, it was reduced at 8 weeks and no longer significant after 24 weeks. In parallel, media cross-section area increased more with time in SHRs than in WKY rats and this was associated with increased contractility and oxidative stress with decreased NO-dependent relaxation. Low flow induced progressive inward remodeling until 24 weeks in both strains with excessive hypertrophy in SHRs. Thus, a chronic increase in flow induced transitory diameter expansion and long-lasting hypertrophy in SHRs. This could contribute to the higher susceptibility of hypertensive subjects to ischemic diseases. Hindawi Publishing Corporation 2014 2014-05-08 /pmc/articles/PMC4034663/ /pubmed/24900916 http://dx.doi.org/10.1155/2014/859793 Text en Copyright © 2014 Odile Dumont et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Dumont, Odile
Kauffenstein, Gilles
Guihot, Anne-Laure
Guérineau, Nathalie C.
Abraham, Pierre
Loufrani, Laurent
Henrion, Daniel
Time-Related Alteration in Flow- (Shear Stress-) Mediated Remodeling in Resistance Arteries from Spontaneously Hypertensive Rats
title Time-Related Alteration in Flow- (Shear Stress-) Mediated Remodeling in Resistance Arteries from Spontaneously Hypertensive Rats
title_full Time-Related Alteration in Flow- (Shear Stress-) Mediated Remodeling in Resistance Arteries from Spontaneously Hypertensive Rats
title_fullStr Time-Related Alteration in Flow- (Shear Stress-) Mediated Remodeling in Resistance Arteries from Spontaneously Hypertensive Rats
title_full_unstemmed Time-Related Alteration in Flow- (Shear Stress-) Mediated Remodeling in Resistance Arteries from Spontaneously Hypertensive Rats
title_short Time-Related Alteration in Flow- (Shear Stress-) Mediated Remodeling in Resistance Arteries from Spontaneously Hypertensive Rats
title_sort time-related alteration in flow- (shear stress-) mediated remodeling in resistance arteries from spontaneously hypertensive rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4034663/
https://www.ncbi.nlm.nih.gov/pubmed/24900916
http://dx.doi.org/10.1155/2014/859793
work_keys_str_mv AT dumontodile timerelatedalterationinflowshearstressmediatedremodelinginresistancearteriesfromspontaneouslyhypertensiverats
AT kauffensteingilles timerelatedalterationinflowshearstressmediatedremodelinginresistancearteriesfromspontaneouslyhypertensiverats
AT guihotannelaure timerelatedalterationinflowshearstressmediatedremodelinginresistancearteriesfromspontaneouslyhypertensiverats
AT guerineaunathaliec timerelatedalterationinflowshearstressmediatedremodelinginresistancearteriesfromspontaneouslyhypertensiverats
AT abrahampierre timerelatedalterationinflowshearstressmediatedremodelinginresistancearteriesfromspontaneouslyhypertensiverats
AT loufranilaurent timerelatedalterationinflowshearstressmediatedremodelinginresistancearteriesfromspontaneouslyhypertensiverats
AT henriondaniel timerelatedalterationinflowshearstressmediatedremodelinginresistancearteriesfromspontaneouslyhypertensiverats