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Obesity‐induced hypertension depends on neurons of the rostral ventrolateral medulla (RVLM)
Author(s) -
Stocker Sean D,
Meador Rachel,
Adams Julye M
Publication year - 2007
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.21.5.a459-c
Subject(s) - rostral ventrolateral medulla , medicine , endocrinology , phenylephrine , muscimol , microinjection , blood pressure , agonist , sympathetic nervous system , obesity , chemistry , receptor , heart rate
Activation of the sympathetic nervous system contributes to obesity‐induced hypertension. The present study determined whether sympathetic neurons of the RVLM contribute to elevated arterial blood pressure (ABP) in obese rats. Male Sprague Dawley rats were placed on a moderately high fat diet (32% kcal, n=24) or a low‐fat diet (LF, 10.6% kcal, n=7). After 14 weeks, rats fed the moderately high fat diet segregated into obesity‐prone (OP) and obesity‐resistant (OR) groups based on their body weight (OP: 869±25, OR: 709±8, LF: 702±33 g; p<0.05). Baseline mean ABP was significantly elevated in OP rats versus OR and LF rats (OP: 108±2, OR: 100±2, LF: 97±3 mmHg; p<0.05). Inhibition of the RVLM with bilateral microinjection of the GABA A receptor agonist muscimol (200 pmol/100 nl) decreased mean ABP to similar levels (OP: 49±1, OR: 50±2, LF: 49±1 mmHg), but the magnitude of this decrease was significantly greater in OP versus OR and LF groups (OP: −58±2, OR: −49±1, LF: −48±3 mmHg; p<0.05). These differences in MAP cannot be explained by changes in vascular reactivity as the ED 50 was not different across groups in response to phenylephrine (OP: 12.2±1.5, OR: 15.0±2.7, LF: 13.8±2.0 μg/kg) or norepinephrine (OP: 1.4±0.1, OR: 1.4±0.2, LF: 1.4±0.1 μg/kg). Blood volume was not different among groups (OP: 45±2, OR: 43±2, LF: 40±2 ml). The present findings suggest that sympathetic neurons of the RVLM contribute to the elevated blood pressure in obese rats.