An F 2 population (n = 151) derived from Dahl salt-sensitive (S) and Lewis rats was raised on a 8% NaCl diet for 9 weeks and analyzed for blood pressure quantitative trait loci (QTL) by use of a whole genome scan. Chromosomes 5 and 10 yielded lod scores for linkage to blood pressure that were significant; chromosomes 1, 2, 3, 8, 16, 17, and 18 gave lod scores suggestive for linkage. Chromosome 7 gave a significant signal for heart weight with a lesser effect on blood pressure. Congenic strains were constructed by introgressing Lewis low-blood-pressure QTL alleles for chromosomes 1, 5, 10, and 17 into the S genetic background. Congenic strains for chromosomes 1, 5, and 10 had significantly lower blood pressure than S, proving the existence of QTL on these chromosomes, but the chromosome 17 congenic strain failed to trap a contrasting QTL allele. The QTL allele increasing blood pressure originated from S rats for all QTL except those on chromosomes 2 and 7 in which the Lewis allele increased blood pressure. Interactions between each QTL and every other locus in the genome scan yielded significant interactions between chromosomes 10 and 4, and between chromosomes 2 and 3.More than 30 years ago, Dahl et al. (1963) selectively bred rats for sensitivity (S rats) and resistance (R rats) to the hypertensive effect of a high-salt (NaCl) diet. Inbred strains of S and R rats were subsequently developed from Dahl's selectively bred lines (Rapp and Dene 1985). These strains are the prototypic animal model for studying salt-induced hypertension.S rats develop hypertension even on a low-salt diet, but this is markedly exacerbated by increased salt intake (Dahl et al. 1963;Rapp and Dene 1985). Chromosomal regions containing blood pressure quantitative trait loci (QTL) have been detected by the candidate gene approach starting in 1972 with a biochemical genetic marker for steroid 11␤-hydroxylase Dahl 1972a, 1976), and then in 1989 when restriction fragment-length polymorphisms first became available (Rapp et al. 1989). More recently, additional chromosomal regions containing blood pressure QTL were identified around candidate genes by use of Dahl rats and more modern genetic markers

The goal of this study was to identify inbred rat strains that could serve as useful models for exploration of the genetic basis of aerobic endurance performance. Six rats of each gender from 11 different inbred strains were tested for 1) maximal running capacity on a treadmill and 2) isolated cardiac performance. Running performance was estimated from 1) duration of the run, 2) distance run, and 3) vertical work performed. Cardiac output, during constant preload and afterload, was taken as a measure of cardiac performance from an isolated working heart preparation. The COP rats were the lowest performers and the DA rats were the best performers by all estimates of running performance. Across the 11 strains, the distance run correlated positively with isolated cardiac performance (r = 0.87). Estimates of performance were as follows (COP vs. DA strain, respectively): duration of run, 19.9 +/- 1.8 vs. 41.5 +/- 2. 2 min; distance run, 298 +/- 30 vs. 840 +/- 64 m; vertical work, 15 +/- 1.7 vs. 40 +/- 4.4 kg/m. These approximately 2.5-fold differences in running performance between the COP and DA suggest that these strains could serve as models for evaluation of the genetic basis of variance in aerobic performance.

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