REGIONAL SYMPATHETIC NERVOUS ACTIVITY AND OXYGEN-CONSUMPTION IN OBESENORMOTENSIVE HUMAN-SUBJECTS

Background Disturbed sympathetic nervous function may be of importance in obesity; sympathetic underactivity could contribute to deficient t hermogenesis, positive energy balance, and weight gain, while in contr ast, sympathetic nervous overactivity would predispose to the developm ent of obesity-related hypertension. Global indices of sympathetic ner vous system (SNS) function such as plasma or urinary norepinephrine (N E) have been unable to define SNS status in obesity. Since regional SN S activity can be altered in the absence of global changes, we investi gated SNS activity in the heart, kidneys, and hepatomesenteric bed in healthy human subjects across a wide body mass index (BMI) range of be tween 19.6 and 35.5. Methods and Results Whole-body and regional plasm a NE kinetics using [H-3]-labeled NE were assessed. Regional oxygen co nsumption was measured by combining arteriovenous differences in oxyge n content and regional blood flow. Arterial plasma NE and whole-body p lasma NE spillover were unrelated to BMI. With a BMI cutoff of 27, mea n cardiac NE spillover was 46% lower in the obese subjects when compar ed with the lean subjects (P=.017). Renal NE spillover was significant ly correlated with BMI (r=.668, P=.001), the mean value in the obese s ubjects being more than twice that in the lean subjects. Hepatomesente ric NE spillover was comparable in lean and obese subjects. Renal and hepatomesenteric oxygen consumption were both significantly higher in the obese subjects compared with lean subjects. Conclusions Regional S NS activity is heterogeneous in the obese state. Important regional al terations, which may be clinically relevant, occur in the absence of c hanges in global indices of sympathetic nervous function. The enhanced renal NE spillover in obesity may have implications for the developme nt of hypertension in this group, whereas the low cardiac sympathetic tone would be expected to be cardioprotective. Enhanced visceral oxyge n consumption evident in the kidneys and hepatomesenteric circulation in proportion to body mass contributes to the greater resting oxygen c onsumption in obesity.