Angiotensin I Infusion Reveals Differential Effects of Angiotensin-Converting Enzyme in Aortic Resident Cells on Aneurysm Formation.

Abstract

BACKGROUND:

Angiotensin (Ang)I is cleaved by angiotensin-converting enzyme (ACE) to generate AngII. The purpose of this study was to determine the roles of ACE in endothelial and smooth muscle cells in aortic aneurysms.Methods and Results:AngI infusion led to thoracic and abdominal aortic aneurysms in low-density lipoprotein receptor-deficient mice, which were ablated by ACE inhibition. Endothelial or smooth muscle cell-specific ACE deletion resulted in reduction of AngI-induced thoracic, but not abdominal, aortic dilatation.

CONCLUSIONS:

AngI infusion causes thoracic and abdominal aortic aneurysms in mice. ACE in aortic resident cells has differential effects on AngI-induced thoracic and abdominal aortic aneurysms.

• Authors: Hisashi Sawada, Masayoshi Kukida, Xiaofeng Chen, Deborah A Howatt, Jessica J Moorleghen, Anju Balakrishnan, Congqing Wu, Alan Daugherty, Hong S Lu
• Journal: Circulation journal : official journal of the Japanese Circulation Society (Circ J) Vol. 84 Issue 5 Pg. 825-829 (04 24 2020) ISSN: 1347-4820 [Electronic] Japan
• PMID: 32238693 (Publication Type: Comparative Study, Journal Article, Research Support, N.I.H., Extramural)

Chemical References

• Angiotensin-Converting Enzyme Inhibitors
• Receptors, LDL
• Angiotensin I
• Peptidyl-Dipeptidase A

Topics

• Angiotensin I
• Angiotensin-Converting Enzyme Inhibitors (pharmacology)
• Animals
• Aorta, Abdominal (drug effects, enzymology, pathology)
• Aorta, Thoracic (drug effects, enzymology, pathology)
• Aortic Aneurysm, Abdominal (chemically induced, enzymology, pathology, prevention & control)
• Aortic Aneurysm, Thoracic (chemically induced, enzymology, pathology, prevention & control)
• Dilatation, Pathologic
• Disease Models, Animal
• Endothelial Cells (enzymology, pathology)
• Mice, Knockout
• Myocytes, Smooth Muscle (enzymology, pathology)
• Peptidyl-Dipeptidase A (deficiency, genetics, metabolism)
• Receptors, LDL (deficiency, genetics)