The inbred Brown Norway (BN) rat presents several rare arterial phenotypes, including an aortic elastin deficit, a high incidence of PDA and the spontaneous formation of ruptures in the internal elastic lamina (RIEL) of the abdominal aorta (AA) and iliac arteries. Our previously performed genetic linkage study, using microsatellite markers, showed that these 3 arterial phenotypes do not correlate in the backcross population and so are independent, and are controlled by distinct genetic loci (Kota et al. Physiol. Genomics, 2007). The RIEL phenotype is of particular interest as it probably reflects a structural anomaly of the elastic network of the AA and the contiguous common iliac arteries. Since the human AA is highly susceptible to pathological alterations with aging, i.e. atherosclerosis and aneurysm formation, for reasons not entirely understood, the discovery of a gene influencing AA elastic network structure would be of interest. In the BN rat, RIEL is strongly linked to a locus on chromosome 5 (peak LOD score 27.4) but in this locus candidate genes are sparse and sequencing them gave negative results. We thus produced congenic rats, introgressing the chrom5 segment containing the RIEL locus from BN rats on a LOU (control) genetic background. These rats express the phenotype sufficiently (30 % of parental BN values) to permit further studies on recombinant offspring to try and locate the gene(s) responsible. We have analysed genotype-phenotype correlations in a large cohort of recombinants, obtained by crossing the congenic rat LOU.BN.D5Rat59-D5Rat131 with parental LOU and subsequent intercrossing, in order to further define the position of the gene(s) responsible. We also performed high-density SNP mapping on chosen, informative recombinants, using >5000 SNPs discriminative between BN and LOU, and demonstrated the purity of the LOU genetic background (>99.9 % outside the chr.5 congenic region). Further generations of recombinants produced from informative genitors and use of SNP genotyping in the congenic region has enabled us to locate the gene(s) responsible for a moderate RIEL phenotype in the first 6Mb region of chrom5. However, BN homozygosity down to 35 Mb causes increased severity of the phenotype.