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Angiotensin II constricts mouse iliac arteries: possible mechanism for aortic aneurysms
LK. Gadanec, KR. McSweeney, P. Kubatka, M. Caprnda, L. Gaspar, R. Prosecky, J. Dragasek, P. Kruzliak, V. Apostolopoulos, A. Zulli
Jazyk angličtina Země Nizozemsko
Typ dokumentu časopisecké články
NLK
ProQuest Central
od 1997-01-01 do Před 1 rokem
Medline Complete (EBSCOhost)
od 2011-01-01 do Před 1 rokem
Health & Medicine (ProQuest)
od 1997-01-01 do Před 1 rokem
- MeSH
- aneurysma břišní aorty * chemicky indukované MeSH
- angiotensin I MeSH
- angiotensin II farmakologie MeSH
- aortální aneurysma * MeSH
- arteria iliaca MeSH
- arterie MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- peptidové hormony * MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Abdominal aortic aneurysms (AAA) result from maladaptive remodeling of the vascular wall and reduces structural integrity. Angiotensin II (AngII) infusion has become a standard laboratory model for studying AAA initiation and progression. We determined the different vasoactive responses of various mouse arteries to Ang II. Ex vivo isometric tension analysis was conducted on 18-week-old male C57BL/6 mice (n = 4) brachiocephalic arteries (BC), iliac arteries (IL), and abdominal (AA) and thoracic aorta (TA). Arterial rings were mounted between organ hooks, gently stretched and an AngII dose response was performed. Rings were placed in 4% paraformaldehyde for immunohistochemistry analysis to quantify peptide expression of angiotensin type 1 (AT1R) and 2 receptors (AT2R) in the endothelium, media, and adventitia. Results from this study demonstrated vasoconstriction responses in IL were significantly higher at all AngII doses when compared to BC, and TA and AA responses (maximum constriction-IL: 68.64 ± 5.47% vs. BC: 1.96 ± 1.00%; TA: 3.13 ± 0.16% and AA: 2.75 ± 1.77%, p < 0.0001). Expression of AT1R was highest in the endothelium of IL (p < 0.05) and in the media and (p < 0.05) adventitia (p < 0.05) of AA. In contrast, AT2R expression was highest in endothelium (p < 0.05), media (p < 0.01, p < 0.05) and adventitia of TA. These results suggest that mouse arteries display different vasoactive responses to AngII, and the exaggerated response in IL arteries may play a role during AAA development.
Australian Institute for Musculoskeletal Science Sunshine Hospital Melbourne VIC 3021 Australia
Faculty of Health Sciences University of Ss Cyril and Methodius in Trnava Trnava Slovakia
Faculty of Medicine Pavol Jozef Safarik University and University Hospital Kosice Slovakia
Institute of Health and Sport Victoria University Werribee Camous Melbourne VIC 3030 Australia
Citace poskytuje Crossref.org
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- $a Abdominal aortic aneurysms (AAA) result from maladaptive remodeling of the vascular wall and reduces structural integrity. Angiotensin II (AngII) infusion has become a standard laboratory model for studying AAA initiation and progression. We determined the different vasoactive responses of various mouse arteries to Ang II. Ex vivo isometric tension analysis was conducted on 18-week-old male C57BL/6 mice (n = 4) brachiocephalic arteries (BC), iliac arteries (IL), and abdominal (AA) and thoracic aorta (TA). Arterial rings were mounted between organ hooks, gently stretched and an AngII dose response was performed. Rings were placed in 4% paraformaldehyde for immunohistochemistry analysis to quantify peptide expression of angiotensin type 1 (AT1R) and 2 receptors (AT2R) in the endothelium, media, and adventitia. Results from this study demonstrated vasoconstriction responses in IL were significantly higher at all AngII doses when compared to BC, and TA and AA responses (maximum constriction-IL: 68.64 ± 5.47% vs. BC: 1.96 ± 1.00%; TA: 3.13 ± 0.16% and AA: 2.75 ± 1.77%, p < 0.0001). Expression of AT1R was highest in the endothelium of IL (p < 0.05) and in the media and (p < 0.05) adventitia (p < 0.05) of AA. In contrast, AT2R expression was highest in endothelium (p < 0.05), media (p < 0.01, p < 0.05) and adventitia of TA. These results suggest that mouse arteries display different vasoactive responses to AngII, and the exaggerated response in IL arteries may play a role during AAA development.
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