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Hypertension. 2008;52:687-695
Published online before print August 11, 2008, doi: 10.1161/HYPERTENSIONAHA.107.109603
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(Hypertension. 2008;52:687.)
© 2008 American Heart Association, Inc.


Original Articles

Dissociation Between Sympathetic Nerve Traffic and Sympathetically Mediated Vascular Tone in Normotensive Human Obesity

Alexei Vasilievich Agapitov; Marcelo Lima de Gusmão Correia; Christine Ann Sinkey; William Geoffrey Haynes

From the Institute for Clinical and Translational Science and Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City.

Correspondence to Marcelo Lima de Gusmão Correia, Clinical Research Unit (157 MRF), University of Iowa Hospitals and Clinics, Iowa City, IA 52242. E-mail marcelo_correia{at}yahoo.com

Obesity increases the risk of hypertension and its cardiovascular complications. This has been partly attributed to increased sympathetic nerve activity, as assessed by microneurography and catecholamine assays. However, increased vasoconstriction in response to obesity-induced sympathoactivation has not been unequivocally demonstrated in obese subjects without hypertension. We evaluated sympathetic {alpha}-adrenergic vascular tone in the forearm by brachial arterial infusion of the {alpha}-adrenoreceptor antagonist phentolamine (120 µg/min) in normotensive obese (daytime ambulatory arterial pressure: 123±1/77±1 mm Hg; body mass index: 35±1 kg/m2) and lean (daytime ambulatory arterial pressure: 123±2/77±2 mm Hg; body mass index: 22±1 kg/m2) subjects (n=25 per group) matched by blood pressure, age, and gender. Microneurographic sympathetic nerve activity to skeletal muscle was significantly higher in obese subjects (30±3 versus 22±1 bursts per minute; P=0.02). Surprisingly, complete {alpha}-adrenergic receptor blockade by phentolamine (at concentrations sufficient to completely inhibit norepinephrine and phenylephrine-induced vasoconstriction) caused equivalent vasodilatation in obese (–57±2%) and lean subjects (–57±3%; P=0.9). In conclusion, sympathetic vascular tone in the forearm circulation is not increased in obese normotensive subjects despite increased sympathetic outflow. Vasodilator factors or mechanisms occurring in obese normotensive subjects could oppose the vasoconstrictor actions of increased sympathoactivation. Our findings may help to explain why some obese subjects are protected from the development of hypertension.


Key Words: obesity • arterial pressure • sympathetic nervous system • vasoconstriction