Published Online
on November 20, 2006

A more recent version of this article appeared on January 1, 2007

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Submitted on August 10, 2006
Revised on August 25, 2006

Autonomic Contribution to Blood Pressure and Metabolism in Obesity

Cyndya Shibao; Alfredo Gamboa; Andre Diedrich; Andrew C. Ertl; Kong Y. Chen; Daniel W. Byrne; Ginnie Farley; Sachin Y. Paranjape; Stephen N. Davis; and Italo Biaggioni^*

From the Division of Clinical Pharmacology and the Autonomic Dysfunction Center (C.S., A.G., A.D., G.F., S.Y.P., I.B.) and Divisions of Gastroenterology (K.Y.C.) and Diabetes, Endocrinology, and Metabolism (A.C.E., S.N.D.), Department of Medicine, and the Department of Biostatistics and the General Clinical Research Center (D.W.B.), Vanderbilt University School of Medicine, Nashville, Tenn.

^* To whom correspondence should be addressed. E-mail: Italo.biaggioni{at}vanderbilt.edu.

Abstract--Obesity is associated with alterations in the autonomic nervous system that may contribute to the increase in blood pressure and resting energy expenditure present in this condition. To test this hypothesis, we induced autonomic withdrawal with the ganglionic blocker trimethaphan in 10 lean (32±3 years) and 10 obese (35±3 years) subjects. Systolic blood pressure fell more in obese compared with lean subjects (-17±3 versus -11±1 mm Hg; P=0.019) because of a greater decrease in total peripheral resistance (-310±41 versus 33±78 dynes/sec/cm^-5; P=0.002). In contrast, resting energy expenditure decreased less in obese than in lean subjects, (-26±21 versus -86±15 kcal per day adjusted by fat-free mass; P=0.035). We confirmed that the autonomic contribution to blood pressure was greater in obesity after including additional subjects with a wider range of blood pressures. Systolic blood pressure decreased -28±4 mm Hg (95% CI: -38 to -18.0; n=8) in obese hypertensive subjects compared with lean (-9±1 mm Hg; 95% CI: -11 to -6; n=22) or obese normotensive subjects (-14±2 mm Hg; 95% CI: -18 to -10; n=20). After removal of autonomic influences, systolic blood pressure remained higher in obese hypertensive subjects (109±3 versus 98±2 mm Hg in lean and 103±2 mm Hg in obese normotensive subjects; P=0.004) suggesting a role for additional factors in obesity-associated hypertension. In conclusion, sympathetic activation induced by obesity is an important determinant to the blood pressure elevation associated with this condition but is not effective in increasing resting energy expenditure. These results suggest that the sympathetic nervous system could be targeted in the treatment of obesity-associated hypertension.

Key words: obesity • hypertension • autonomic nervous system • sympathetic nervous system • vascular resistance • metabolism

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