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. Author manuscript; available in PMC: 2014 Mar 1.
Published in final edited form as: CNS Drugs. 2013 Mar;27(3):221–232. doi: 10.1007/s40263-013-0051-4

Table 1.

Evidence for altered noradrenergic function in PTSDa

Physiological observations Study results
Baseline/resting state measures
 Increased resting heart rate and blood pressure +/−
 Increased resting urinary noradrenaline
(norepinephrine) and adrenaline (epinephrine)
+
 Decrease in basal and stimulated activity of cAMP +/−
 Decreased binding to platelet α2 receptors +
 Decrease in platelet MAO activity +
 Increased resting plasma noradrenaline or MHPG +/−
Challenge test markers
 Increased plasma noradrenaline with traumatic
reminders/panic attacks
+
 Increased heart rate and blood pressure response to
traumatic reminders/panic attacks
+++
 Increased orthostatic heart rate response to exercise +
 Increased symptoms, heart rate and plasma MHPG
with yohimbine noradrenergic challenge
++
 Differential brain metabolic response to yohimbine +
a

The evidence for altered noradrenergic functioning in PTSD is stronger in challenge test designs (i.e., incorporating threat responses, trauma reminders) in comparison to baseline/resting state studies

cAMP cyclic adenosine 3′5′-monophosphate, MAO monoamine oxidase, MHPG 3-methosy-4-hydroxyphenylglycol, PTSD post-traumatic stress disorder, +/− indicates an equal number of studies support this finding and do not support this finding, + indicates at least one study supports this finding and no studies do not support the finding, or the majority of studies support the finding, ++ indicates two or more studies support this finding, and no studies do not support the finding, +++ indicates three or more studies support this finding, and no studies do not support the finding