title: Autonomic contribution to blood pressure and metabolism in obesity.
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.
authors.affiliation: Division of Clinical Pharmacology and the Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, TN 37212, USA.
authors.forename: Cyndya
authors.initials: C
authors.lastname: Shibao
authors.forename: Alfredo
authors.initials: A
authors.lastname: Gamboa
authors.forename: Andre
authors.initials: A
authors.lastname: Diedrich
authors.forename: Andrew C
authors.initials: AC
authors.lastname: Ertl
authors.forename: Kong Y
authors.initials: KY
authors.lastname: Chen
authors.forename: Daniel W
authors.initials: DW
authors.lastname: Byrne
authors.forename: Ginnie
authors.initials: G
authors.lastname: Farley
authors.forename: Sachin Y
authors.initials: SY
authors.lastname: Paranjape
authors.forename: Stephen N
authors.initials: SN
authors.lastname: Davis
authors.forename: Italo
authors.initials: I
authors.lastname: Biaggioni
mesh_terms: D000328:Adult; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001794:Blood Pressure / Q000187:drug effects; D002319:Cardiovascular System / Q000187:drug effects / Q000503:physiopathology; D004734:Energy Metabolism / Q000187:drug effects; D005260:Female; D005730:Ganglionic Blockers / Q000494:pharmacology; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D009765:Obesity / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D012146:Rest; D013599:Systole; D013851:Thinness / Q000378:metabolism / Q000503:physiopathology; D014294:Trimethaphan / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D005730:Ganglionic Blockers; D014294:Trimethaphan