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1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA; Department of Human and Molecular Genetics, Medical College of Wisconsin, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: dmattson{at}mcw.edu.
Linkage analysis studies previously identified genetic loci associated with proteinuria and hypertension on chromosome 1 of FHH (Fawn Hooded Hypertensive) rats. The present studies were performed on conscious male and female rats to evaluate the influence of transfer of chromosome 1 from the BN (Brown Norway) rat to the FHH genetic background (FHH-1BN). Rats were maintained for two weeks on 8.0% NaCl chow with L-NAME in the drinking water (12.5 mg/l) to induce hypertension and accelerate the onset of renal disease. Mean arterial blood pressure (MAP) was significantly higher in the male FHH (188±3 mmHg, n=13) in comparison to the BN (121±3 mmHg, n=8); MAP in the FHH-1BN was midway between the two parental strains (167±5 mmHg, n=9). Urinary protein and albumin excretion rates in the male FHH-1BN (Uprot=189±36 mg/day, Ualb=69±16 mg/day, n=10) were also midway between levels observed in the FHH (Uprot=485±54 mg/day; Ualb= 206±25 mg/day, n=13) and the BN (Uprot=32±5 mg/day, Ualb=5±1 mg/day, n=8). Creatinine clearance was elevated, and the degree of glomerular damage was significantly reduced in the FHH-1BN compared to the FHH. Qualitatively similar results were obtained from female FHH, FHH-1BN and BN rats. The present results indicate that genes contributing to L-NAME-induced hypertension and renal disease are found on chromosome 1 of the FHH rat.
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