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The aim of this study was to determine whether elements of the human renin-angiotensin system (RAS) could function-ally replace elements of the mouse RAS by complementing the reduced survival and renal abnormalities observed in mice carrying a gene-targeted deletion of the mouse angio-tensinogen gene ( mAgt). Double transgenic mice containing the human renin ( HREN) and human angiotensinogen HAGT) genes were bred to mice heterozygous for the mAgt deletion and the compound heterozygotes were identified and intercrossed. The resulting progeny (