Premium
Strain‐dependent variation in vasoreactivity in isolated mouse thoracic aorta
Author(s) -
Kim Seung Kyum,
Avila Joshua J.,
Massett Michael P.
Publication year - 2012
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.26.1_supplement.1098.12
Subject(s) - phenylephrine , sodium nitroprusside , strain (injury) , aorta , thoracic aorta , snp , acetylcholine , inbred strain , medicine , chemistry , endocrinology , endothelium , biology , single nucleotide polymorphism , biochemistry , gene , nitric oxide , blood pressure , genotype
Understanding genetic influence on vascular reactivity is important for identifying genes underlying impaired vascular function. Therefore, the aim of this study was to characterize genetic variation in vascular reactivity using 14 inbred strains of mice. Concentration response curves to phenylephrine (PE), potassium chloride (KCl), acetylcholine (ACh), and sodium nitroprusside (SNP) were obtained from aortic rings from male mice (n ≈ 4/strain). Contractile responses to PE and KCl varied significantly across strains. In response to PE, aorta from PWD/PhJ had the lowest (43.8 ± 6.7 %) and aorta from NZW/LacJ had the highest (160.8 ± 15.6 %) maximal response. Aorta from C57BL/6J and 129S1/SvImJ had the lowest (112.0 ± 19.8 %) and the highest (183.2 ± 5.5 %) maximal response to KCl, respectively. Endothelium‐dependent relaxation responses to ACh were also significantly different across strains with NZW/LacJ having the lowest (50.1 ± 7.7 %) and C3H/HeJ having the highest (98.6 ± 0.5 %) maximal response. Maximal endothelium‐independent relaxation responses to SNP were similar among strains. Differences in sensitivity to all agents were observed across strains. These data demonstrate that there are large strain‐dependent differences in vasoreactivity across inbred mouse strains and indicates that genetic background influences vascular function. Supported by NIH grant HL085918 to MPM