Why the study?
Does neuroadrenergic stimulation produced by orthostatic stress affect plasma free fatty acid concentration in humans?
Does neuroadrenergic stimulation produced by orthostatic stress affect plasma free fatty acid concentration in humans?
This study investigates the physiological role of the sympathetic nervous system in mobilizing free fatty acids during orthostatic stress.
No immediate clinical implications for orthostatic intolerance; leaves open sympathetic control of lipolysis in humans.
A role of the sympathetic nervous system in the metabolism of adipose tissue has been suggested by clinical observations and by animal denervation experiments (1). The recent observations of the mobilization of free fatty acids' (FFA) by norepinephrine (NE) in vitro (2) and in vivo (3, 4) add presumptive evidence for a function of the sympathetic nervous system in the transport of fatty acids. To elucidate further the role of the sympathetic nervous system in fatty acid transport, the effect of a standard physiological stress on plasma FFA concentration was studied. Previous work has shown that the normal individual defends against the orthostatic stress of a 60° upright tilt by an increase in diastolic blood pressure and pulse rate. This response is probably mediated by the autonomic nervous system through baroceptor reflexes and is accompanied by a rise in plasma NE concentration (5). These responses reflect an increase in neuroadrenergic activity; and, as a corollary, are absent in individuals after sympathectomy and in patients with primary autonomic insufficiency. It is the purpose of this report to present the effects of neuroadrenergic stimulation produced by orthostatic stress on plasmaFFA concentration.
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Hamlin et al. (1960) studied this question.
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