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1 Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
2 Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States; Biotechnology and Bioengineering Center, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
3 Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
4 Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States; Human Molecular and Genetics Center, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
* To whom correspondence should be addressed. E-mail: dmattson{at}mcw.edu.
This study examined the genetic basis for hypertension and renal disease phenotypes in FHH rats using chromosome substitution strains (consomic rats) in which each of the 20 autosomes as well as the X and Y chromosomes were transferred from the normal BN (Brown Norway) rat onto the FHH genetic background. Male and female rats of each parental and consomic strain were maintained for two weeks on high salt (8.0% NaCl) chow with NG-nitro-L-arginine methyl ester (L-NAME) in the drinking water (12.5 mg/l) to induce hypertension and renal disease. Mean arterial blood pressure (MAP) was significantly higher (by over 60 mmHg) in male FHH compared to BN rats. Urinary protein and albumin excretion rates were increased by 15-fold and 40-fold, respectively, in the male FHH compared to the BN. Plasma renin activity was 10-fold higher in the FHH than the BN. Similar significant differences were observed between the female FHH and BN, but the degree of hypertension and proteinuria was of a lesser magnitude. Substitution of chromosome 20 from the BN to the FHH attenuated the development of L-NAME-induced hypertension, normalized plasma renin activity, and decreased plasma creatinine in male rats. In female rats, substitution of chromosome 15 decreased MAP and urinary protein excretion. Urinary excretion of albumin in males was decreased by substitution of chromosomes 1, 15, 16, and 18 from the BN into the FHH genetic background. The present data indicate that genes that can modify L-NAME-induced hypertension and proteinuria are on chromosomes 1, 15, 16, 18 and 20.
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