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Deficiency of epidermal growth factor receptor prevents angiotensin II‐induced hypertrophy, but not inward remodeling, in cerebral arterioles
Author(s) -
Baumbach Gary L,
Gerhold Thomas D
Publication year - 2013
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.27.1_supplement.1182.4
Subject(s) - medicine , endocrinology , angiotensin ii , muscle hypertrophy , autophosphorylation , epidermal growth factor receptor , in vivo , saline , chemistry , arteriole , receptor , biology , microcirculation , biochemistry , protein kinase a , microbiology and biotechnology , enzyme
We examined the effect of epidermal growth factor receptor (EGFR) deficiency on structural alternations in cerebral arterioles induced by angiotensin II (Ang II). Two month old homozygous (−/−) waved‐2 (Wav2) mice, in which a point mutation impairs autophosphorylation of EGFR, and heterozygous (+/−) Wav2 littermates were infused with Ang II (1000 ng/kg/day) or saline via osmotic minipumps for 28‐days. Systolic arterial pressure (SAP) was measured by a tail‐cuff method. External diameter (ED) of maximally dilated (EDTA) cerebral arterioles was measured in vivo under anesthetized conditions. Cross‐sectional area of the arteriolar wall (CSA) was measured histologically. Ang II increased SAP pressure in Wav2+/− (142±4 vs 115±5 mmHg in saline infused, P<0.05) and Wav2−/− mice (136±6 vs 108±5 mmHg, P<0.05). ED was reduced by Ang II in both Wav2+/− (58±3 vs 69±3 μm, P<0.05) and Wav2−/− (59±3 vs 68±4 μm, P<0.05) mice, whereas CSA was increased in Wav2+/− (518±56 vs 403±35 μm 2 , P<0.05), but not in Wav2−/− (410±24 vs 419±65 μm 2 , P<0.05), mice. These findings suggest that transactivation of EGFR may play an important role in Ang II‐induced hypertrophy of cerebral arterioles, but may not in inward remodeling.