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Brown Norway chromosome 16 protects the SS‐16BN/Mcwi consomic model of left ventricular hypertrophy from progressing to heart failure
Author(s) -
Kriegel Alison Jessica,
Greene Andrew S.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1130.17
Subject(s) - left ventricular hypertrophy , ejection fraction , fibrosis , heart failure , medicine , introgression , cardiology , muscle hypertrophy , endocrinology , phenotype , blood pressure , chromosome , genetic model , biology , gene , genetics
Left ventricular hypertrophy (LVH) is a well established risk factor for cardiovascular disease however the determinants of progression to heart failure (HF) have been incompletely characterized. Regulatory pathways are difficult to study in humans due to the interaction of genetic and environmental factors. Selective breeding of animal models allows for tight control of these factors. We find that introgression of chromosome 16 from the normotensive Brown Norway (BN) rat onto the genetic background of the hypertensive SS/Mcwi (Dahl Salt‐Sensitive (SS)) both reduces blood pressure and prevents HF in the consomic SS‐16 BN /Mcwi (SSBN16) rat, a model of idiopathic LVH. LV fibrosis and ejection fraction (EF) were both measured at 18 and 36 weeks of age in the SS, SSBN16 and BN rats as indicators of progressive HF. At 18 weeks the percent of the LV showing fibrosis did not differ between strains, but by 36 weeks both the SS and BN rats exhibited a significant increase (122% and 78% respectively; p < 0.05, ANOVA). There was no change in fibrosis in the SSBN16. EF was preserved near 85% in the SSBN16 and BN rats between 18 and 36 weeks, while it dropped in the SS rats from 84.81% ± 2.45 to 60.74% ± 4.11. This data suggests that the interaction of one or more genes on BN chromosome 16 with the SS genetic background protects the LV from developing phenotypes associated with HF and may be part of a HF regulatory pathway. Support HL 29587; HL 66579