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SUMMARY For circulating norepinephrine (NE) to reflect sympathetic activity validly, plasma NE should show an intensity-dependent increase during sympathetic stimulation and decrease during sympathetic inhibition, and circulating NE should correlate with more directly obtained measures of sympathetic activity. Review of published evidence indicates that NE in peripheral plasma satisfies these criteria. However, models used to explain the relationship between circulating NE and sympathetic activity must take into account processes intervening between the synaptic cleft and free NE in the circulation and, since sympathetic outflow is regionalized, the contributions of specific vascular beds to circulating NE. In this report a model is presented where removal processes for NE are viewed as acting in series to produce a gradient in NE concentrations from synapse to plasma, and where the relative contributions of specific vascular beds are calculated from the arteriovenous difference in plasma NE across those beds and the percentage of cardiac output distributed to them. In general, venous plasma NE provides a useful estimation of average sympathetic outflow. (Hypertension 5: 552-559, 1983) KEY WORDS • norepinephrine • epinephrine • catecholamines • sympathetic nervous system • hypertension • spontaneously hypertensive rat M ANY recent studies have used venous plasma norepinephrine (NE) concentrations as an index of sympathetic neural activity in humans, and several of these studies have reported plasma NE to be increased in some patients -in particular, young patients -with essential hypertension.1 -2 In general, these studies have not critically evaluated the relationship between sympathetic outflow and circulating NE. An understanding of the factors determining that relationship is crucial for interpreting NE levels in terms of sympathetic neural activity in disease states such as essential hypertension. In this report we discuss the validity of antecubital venous plasma NE for clinical evaluation of sympathetic function, taking into account the factors known to intervene between sympathetically mediated NE release and levels of NE in venous plasma.For circulating NE to be a valid reflection of sympathetic activity, several criteria must be met: 1) during stimulation of sympathetic outflow, plasma NE should From the National Heart, Lung, and Blood Institute (Dr. Goldstein); the Laboratory of Clinical Science, National Institute of Mental Health (Drs. Polinsky and Kopin), National Institutes of Health, Bethesda, Maryland; and the Department of Psychology, University of Virginia, Charlottesville, Virginia (Dr. McCarty).Address for reprints: National Heart, Lung, and Blood Institute, NIH, Building 10 8C116, Bethesda, Maryland 20205. Received November 17, 1982; revision accepted January 25, 1983. increase in proportion to the intensity of stimulation; 2) during inhibition of sympathetic outflow, plasma NE should decrease, with the extent of decrease similarly related to the extent of inhibition; and 3) plasma ...

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A comparison was made of the dynamics of sympathoadrenal activity in 11 age-matched male and female rats, under basal conditions and after exposure to footshock. Rats were prepared with indwelling catheters in the tail artery 24 h before the experiment. Measurements were made of plasma corticosterone (COR), norepinephrine (NE), epinephrine (EPI), dihydroxyphenylalanine (DOPA), dihydroxyphenylglycol (DHPG) and dihydroxyphenylacetic acid (DOPAC) under resting conditions, after transfer to the shock box (novelty) and at various times after footshock. Under basal conditions, males have significantly higher blood pressure and plasma DHPG/NE ratios but lower plasma levels of COR, NE and DOPAC than females. Three min after exposure to the shock chamber (novelty stress) there were significant increases in COR, EPI, NE and DHPG in both sexes, while DOPA increased only in females and DOPAC remained unchanged in both sexes. Footshock produced a further increase in EPI, NE and DOPAC within 2 min, which lasted about 15 min. There were significant sex differences in the extent and duration of the response of COR, EPI and DHPG. The data show that the female sympathoadrenal system is more reactive than that of the male to the stresses of a novel environment and footshock. The smaller DHPG/NE ratios in females at rest and after stress suggest that neuronal uptake of NE is lower in females than in males. The finding that stress produces larger increments of plasma DOPA and DOPAC in female rats indicates that tyrosine hydroxylase in the sympathetic nerve terminals and adrenal medulla may also be higher than in males.

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In this review, nonassociative learning is advanced as an organizing principle to draw together findings from both sympathetic-adrenal medullary and hypothalamic-pituitary-adrenocortical (HPA) axis responses to chronic intermittent exposure to a variety of stressors. Studies of habituation, facilitation and sensitization of stress effector systems are reviewed and linked to an animal's prior experience with a given stressor, the intensity of the stressor and the appraisal by the animal of its ability to mobilize physiological systems to adapt to the stressor. Brain pathways that regulate physiological and behavioral responses to stress are discussed, especially in light of their regulation of nonassociative processes in chronic intermittent stress. These findings may have special relevance to various psychiatric diseases, including depression and post-traumatic stress disorder (PTSD).