. Author manuscript; available in PMC: 2012 Mar 1.

Published in final edited form as: N Am J Med Sci (Boston). 2011 Oct 1;4(4):183–190. doi: 10.7156/v4i4p183

Table 1.

Characteristics of mice with genetic manipulations of AGT

Manipulation	Strategy	Pathophysiological Features				References
Manipulation	Strategy	BP	kidney	heart	Others	References
rat Agt overexpression	rat Agt transgene under the control of the mouse metallothionein I promoter	↔	ND	ND	ND	[61]
rat Agt overexpression	rat Agt transgene under the control of the rat Agt promoter	↑	nephro- sclerosis	hyper- trophy	ND	[62,76]
human Agt overexpression	human Agt transgene under the control of the human Agt promoter	↔	↔	↔	↔	[63]
rat Agt and Ren overexpression	breeding of rat Agt transgenic mice with rat Ren transgenic mice	↑	ND	ND	ND	[61]
human Agt and Ren overexpression	breeding of human Agt transgenic mice with human Ren transgenic mice	↑	nephro- sclerosis	hyper- trophy	↓ body weight	[64,94]
whole body Agt deficiency (Agt −/−)	insertion of a neo cassette to the exon 2 prior to the start codon of the mouse Agt	↓	hydro- nephrosis	cardio- myopathy	↓ body weight, fat mass & locomoter activity	[65,66]
rat Agt overexpression in adipocytes	rat Agt transgene under the control of aP2 promoter in wild type mice	↑	ND	ND	↑ body weight & fat mass, ↓ energy expenditure	[79]
rat Agt adipocyte- specific expression	rat Agt transgene under the control of aP2 promoter in Agt −/− mice	↔	↔	ND	↑ body weight & fat mass, ↓ energy expenditure	[79]
Agt adipocyte-specific deficiency	breeding of Agt floxed mice with trangenic mice expressing Cre recombinase under the control of aP2 promoter	↓ in aged mice	ND	ND	↔ body weight & fat mass	[34]

Notes: Agt = angiotensinogen gene; Ren = renin gene; BP = blood pressure; ↔ = no change; ↑ = increase; ↓ = decrease; ND = not determined. The pathophysiological changes were determined in comparison with their relative wild type littermates