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Obesity impairs alpha 1 adrenergic receptor mediated contraction in carotid arteries
Author(s) -
Dorrance Anne McLaren,
McClain Jonathon L
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.866.6
Subject(s) - medicine , endocrinology , contraction (grammar) , phenylephrine , mesenteric arteries , thromboxane , adrenergic , agonist , thromboxane a2 , receptor , artery , blood pressure , platelet
Hypertension is generally thought to cause a hyper contractile state in arteries. This does not appear to be the case in aorta from rats with diet‐induced obesity associated hypertension. We tested the hypothesis that contractile responses would also be impaired in carotid arteries from rats fed a high fat (HF) diet. Male Sprague Dawley rats received a HF diet from 3–20 weeks of age; control rats were fed normal chow (n=4). Carotid arteries were removed and isometric force generation was measured in response to phenylephrine (PE) and the thromboxane A2 receptor agonist U46619. The HF rats were heavier than the controls (401±9 vs 465±10g, control vs HF p<0.05) and had more abdominal fat (5.6±0.3 vs 16.5±1.2g, control vs HF p<0.05). The PE mediated contraction was impaired in carotids from the HF rats as evidenced by an increase in the EC 50 and a reduction in the maximum contraction. This was not the case for U46619 where the responses were similar in the control and HF rats. These studies suggest that alpha 1 adrenergic receptor mediated contraction is impaired by a HF diet; this may be linked to the increased sympathetic drive observed with obesity.PE U46619Max contraction (mN) EC 50 Max contraction (mN) EC 50Control 8.3±0.4 −7.0±0.1 20.4±0.6 −8.0±0.3 HF 6.8±0.6 * −6.7±0.1 * 20.0±0.7 −7.8±0.4* Different from control