Human obesity is characterized by profound alterations in the hemodynamic and metabolic states. Whether these alterations involve sympathetic drive is controversial. In 10 young obese subjects (body mass index, 40.5 +/- 1.2 kg/m2, mean +/- SEM) with normal blood pressure and 8 age-matched lean normotensive control subjects, we measured beat-to-beat arterial blood pressure (Finapres technique), heart rate (electrocardiogram), postganglionic muscle sympathetic nerve activity (microneurography at the peroneal nerve), and venous plasma norepinephrine (high-performance liquid chromatography). The measurements were performed in baseline conditions and, with the exception of plasma norepinephrine, during baroreceptor stimulation and deactivation caused by increases and reductions of blood pressure via intravenous infusions of phenylephrine and nitroprusside. Baseline blood pressure and heart rate were similar in obese and control subjects. Plasma norepinephrine was also similar in the two groups. Muscle sympathetic nerve activity, however, was 38.6 +/- 5.1 bursts per minute in obese subjects and less than half that level in control subjects (18.7 +/- 1.3 bursts per minute), the difference being highly statistically significant (P < .02). Muscle sympathetic nerve activity and heart rate were reduced during phenylephrine infusion and increased during nitroprusside infusion, but the changes were about half as great in obese subjects as in control subjects. 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 complications seen in obesity.
In obese normotensive subjects, a reduction in body weight induced by a hypocaloric diet with normal sodium content exerts a marked reduction in sympathetic activity owing to central sympathoinhibition. This can be due to the consequences of an increased insulin sensitivity but also to a restoration of the baroreflex control of the cardiovascular system with weight loss.
Abstract-Essential hypertension, obesity, and congestive heart failure are characterized by an increase in muscle sympathetic nerve activity. Whether in these conditions skin sympathetic nerve activity is also increased has never been systematically examined, however. In 10 untreated mild essential hypertensive, 12 untreated normotensive obese, 10 mild (New York Heart Association class II) heart failure, and 10 normotensive lean healthy control subjects, we measured beat-to-beat arterial blood pressure (Finapres technique), body mass index, and postganglionic sympathetic nerve activity in skeletal muscle and skin areas (microneurographic technique, peroneal nerve). The muscle and skin nerve measurements were made in a randomized sequence. All data were obtained with the subject supine in a quiet, semidark environment at constant temperature over two periods of 30 minutes each, separated by a 20-to 30-minute interval. Blood pressure was increased only in hypertensive and body mass index only in obese subjects. Muscle sympathetic nerve activity quantified as bursts/min was markedly and significantly (PϽ.01) greater in essential hypertensive (33.3Ϯ1.7), obese (42.2Ϯ2.8), and congestive heart failure subjects (55.8Ϯ4.3) in comparison with control subjects (23.9Ϯ1.6). This was the case also for muscle sympathetic nerve activity, quantified as bursts per 100 heart beats. In contrast, skin sympathetic nerve activity (bursts per minute) was superimposable in hypertensive, obese, heart failure, and control subjects, its ability to increase being documented in all four groups by the marked response to an acoustic stimulus. Thus, in various diseases, muscle but not skin sympathetic activity is increased, with the sympathetic activation not being uniformly distributed over the whole cardiovascular system. (Hypertension. 1998;31[part 1]:64-67.)Key Words: hypertension, essential Ⅲ obesity Ⅲ heart failure Ⅲ sympathetic nervous system Ⅲ reflex M icroneurographic studies have provided evidence that different mechanisms are involved in the regulation of muscle sympathetic nerve activity, ie, that while the former is under baroreflex and humoral control, the latter is mainly modulated by thermoregulatory and emotional factors. [1][2][3][4] This provides a physiological background to the recent finding that in severe heart failure, ie, a condition known to be characterized by a baroreflex impairment and neurohumoral abnormalities, 5-7 sympathetic activation can be detected via microneurography in the muscle but not in the skin nerve areas.8 It remains unsettled, however, whether the different behavior of muscle and skin sympathetic nerve activity reported in heart failure is peculiar to this condition or is a finding commonly observed in other abnormal states characterized by muscle sympathetic activation and reflex and humoral alterations.To obtain conclusive information on this issue, we systematically used the microneurographic technique to assess muscle and skin nerve activity in (1) essential hypertensive patients in which sev...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.