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(Hypertension. 2003;42:96.)
© 2003 American Heart Association, Inc.

Scientific Contributions

Sustained Activation of the Central Baroreceptor Pathway in Obesity Hypertension

From the Departments of Physiology (T.E.L.) and Anatomy (S.W.), University of Mississippi Medical Center Jackson, Miss; and the Department of Physiology (J.T.C.), University of Missouri School of Medicine, Columbia, Mo.

Correspondence to Thomas E. Lohmeier, PhD, Department of Physiology, University of Mississippi Medical Center, 2500 North State St, Jackson, MS 39216-4505. E-mail tlohmeier{at}physiology.umsmed.edu

The major goal of this study was to determine whether there is increased activation of medullary neurons that participate in the central baroreceptor reflex pathway in dogs with obesity-induced hypertension, a model of hypertension that is associated with increased sympathetic activity. We used Fos-like (Fos-Li) protein immunohistochemical methods to determine activation of neurons in the nucleus tractus solitarius (NTS), caudal ventrolateral medulla (CVLM), and rostral ventrolateral medulla (RVLM). Dogs were fed either a regular diet or an identical diet with the addition of 0.5 to 0.9 kg of cooked beef fat. After 6 weeks of the high fat diet, body weight (36.3±0.4 vs 21.5±0.5 kg), mean arterial pressure (105±4 vs 91±3 mm Hg), and heart rate (97±4 vs 70±3 bpm) were significantly greater in obese than in control dogs, respectively. There was little Fos-Li immunoreactivity in medullary neurons of control dogs but marked reactivity in obese dogs. Specifically, the number of Fos-Li–positive cells in the NTS and CVLM was 3 to 5 times greater in obese than in control dogs. Furthermore, despite sustained activation of these baroreceptor-sensitive neurons, there was a significantly greater number of Fos-Li positive cells in the RVLM of dogs fed the high fat diet. As baroreceptor suppression of sympathoexcitatory cells in the RVLM is mediated by activation of neurons in the NTS and CVLM, these results support recent findings indicating that baroreflex suppression of sympathetic activity is a long-term compensatory response in hypertension. However, sympathoexcitatory inputs onto RVLM neurons would appear to predominate over the inhibitory effects of the baroreflex in obesity hypertension.

Key Words: angiotensin • hypertension, obesity • baroreflex • central nervous system • brain

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