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Dahl salt‐sensitive rats on a high‐fat diet develop hypertension and enhanced constriction to angiotensin II without changing endothelial‐dependent vasorelaxation
Author(s) -
Spradley Frank T,
Pollock David M,
Pollock Jennifer S
Publication year - 2010
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.24.1_supplement.1025.9
Subject(s) - medicine , endocrinology , vasoconstriction , constriction , phenylephrine , angiotensin ii , sodium nitroprusside , endothelial dysfunction , blood pressure , chemistry , vasodilation , nitric oxide
Experiments were designed to test the hypothesis that genetic salt‐sensitivity is associated with hypertension and vascular dysfunction under conditions of a high‐fat diet. We established a breeding colony of Dahl salt‐sensitive rats at the Medical College of Georgia (SS/Mcg) that are genotypically similar to SS/Mcw rats. Mean arterial pressure (MAP) was determined by telemetry in SS/Mcg rats on a high‐fat, normal‐salt diet (HF; 59% calories from fat; 0.4% NaCl) and compared to SS.BN13 genetic controls. SS/Mcg rats were hypertensive following 4 wk of HF (152 ± 5 mmHg; n=5) compared to SS/Mcg on a normal diet (ND; 15% calories from fat; 0.4% NaCl) (133 ± 6 mmHg; p<0.05; n=4). MAP in SS.BN13 rats was unchanged by HF (n=4). Vasorelaxation to acetylcholine and nitroprusside as well as vasoconstriction to KCl and phenylephrine were similar in aortic rings from HF and ND SS/Mcg and SS.BN13. In contrast, vasoconstriction in response to Ang II was enhanced in aortic rings from HF SS/Mcg compared to HF SS.BN13 (% maximum constriction: 30 ± 4 (n=5) vs. 2 ± 1 (n=6); p<0.05). However, SS/Mcg and SS.BN13 on ND had similar Ang II‐induced constriction (% maximum constriction: 11 ± 4 (n=5) vs. 13 ± 5 (n=6), respectively; p>0.05). In conclusion, a salt‐sensitive genotype predicts the MAP and Ang II vasoconstrictor response following a short‐term HF diet without promoting endothelial dysfunction. Supported by NIH: HL69999 and HL076146.