Hypertension, Vol 5, 552-559, Copyright © 1983 by American Heart Association
DS Goldstein, R McCarty, RJ Polinsky and IJ Kopin
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.
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Relationship between plasma norepinephrine and sympathetic neural activity
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