September 27, 2007AJP Renal Physiology

Chromosomal mapping of the genetic basis of hypertension and renal disease in FHH rats

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Population

Male and female Fawn Hooded hypertensive rats, Brown Norway rats, and consomic strains maintained on…

Comparison

Chromosome substitution vs Parental FHH and BN strains

Design

Preclinical

Follow-up

2 weeks

Authors

DMDavid L. MattsonAugusta University MDMelinda R. DwinellMedical College of Wisconsin AGAndrew S. GreeneAtrium Health Wake Forest Baptist

Discussion

Member takes

Implication

Candidate loci for hypertension and proteinuria modifiers identified in rats; leaves open human translation and mechanism validation.

Structured PICO

Population

Male and female Fawn Hooded hypertensive (FHH) rats, Brown Norway (BN) rats, and consomic strains maintained on high-salt (8.0% NaCl) chow with l-NAME (12.5 mg/l) in drinking water to induce hypertension and renal disease

Intervention

Chromosome substitution (transfer of each of the 20 autosomes and X/Y chromosomes from normal BN rat onto FHH genetic background)

Comparator

Parental FHH and BN strains

Outcome

Mean arterial blood pressure (MAP), urinary protein and albumin excretion rates, plasma renin activity, and plasma creatininesurrogate

Chromosomal mapping in FHH rats identifies chromosomes 1, 15, 16, 18, and 20 as harboring genes that modify l-NAME-induced hypertension and proteinuria.

Cite This Study

Mattson et al. (2007) studied this question.

synapsesocial.com/papers/6a7609c1d5b06e2c1e613c08 https://doi.org/10.1152/ajprenal.00012.2007

Topics

Hypertension management

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