SYMPATHETIC ACTIVATION IN OBESE NORMOTENSIVE SUBJECTS

Human obesity is characterized by profound alterations in the hemodyna mic and metabolic states. Whether these alterations involve sympatheti c drive is controversial. In 10 young obese subjects (body mass index, 40.5+/-1.2 kg/m(2), mean+/-SEM) with normal blood pressure and 8 age- matched lean normotensive control subjects, we measured beat-to-beat a rterial blood pressure (Finapres technique), heart rate (electrocardio gram), postganglionic muscle sympathetic nerve activity (microneurogra phy at the peroneal nerve), and venous plasma norepinephrine (high-per formance liquid chromatography). The measurements were performed in ba seline conditions and, with the exception of plasma norepinephrine, du ring baroreceptor stimulation and deactivation caused by increases and reductions of blood pressure via intravenous infusions of phenylephri ne and nitroprusside. Baseline blood pressure and heart rate were simi lar in obese and control subjects. Plasma sympathetic nerve activity, however, was 38.6+/-5.1 bursts per minute in obese subjects and less t han half that level in control subjects (18.7+/-1.3 bursts per minute) , the difference being highly statistically significant (P<.02). Muscl e sympathetic nerve activity and heart rate were reduced during phenyl ephrine infusion and increased during nitroprusside infusion, but the changes were about half as great in obese subjects as in control subje cts. Thus, even in the absence of any blood pressure alteration, human obesity is characterized by a marked sympathetic activation, possibly because of an impairment of reflex sympathetic restraint. This may be involved in the high rate of hypertension and cardiovascular complica tions seen in obesity.