Angiotensin II constricts mouse iliac arteries: possible mechanism for aortic aneurysms

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 (AT(1)R) and 2 receptors (AT(2)R) 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 AT(1)R 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, AT(2)R 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.

Automated summary

Abdominal aortic aneurysms (AAA) are caused by abnormal remodeling of the vascular wall and have different vasoactive responses to Angiotensin II (AngII). This study found that mouse arteries have different responses to AngII, with iliac arteries showing significantly higher vasoconstriction responses, which may play a role in AAA development.