These AT1aflox mutant mice possess a loxP site upstream of exon 3 followed by a neomycin resistance (neo) cassette flanked by frt sites and loxP sites downstream of exon 3 of the angiotensin II receptor, type 1a (Agtr1a) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. AGTR1A is expressed in vascular cells such as endothelial cells, smooth muscle cells, and macrophages. Angiotensin II (Ang II) is a vasoconstrictor which, upon binding to AGTR1A, can induce aneurysms in the ascending aorta. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exon 3 deleted in the cre-expressing tissues. When this floxed strain is crossed to a strain expressing Cre recombinase in smooth muscle, deletion of Agtr1a had no affect on ascending aortic aneurysms (AA) after Ang II infusion. In contrast, when crossed to a strain expressing Cre recombinase in endothelial cells, deletion of Agtr1a resulted in a reduction in ascending AA after Ang II infusion. This strain may be useful for studying the role of cell specific Agtr1a expression on ascending AA.
