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Association of Depressive and Anxiety Symptoms With 24-Hour Urinary Catecholamines in Individuals With Untreated High Blood Pressure

Paine, Nicola J. PhD; Watkins, Lana L. PhD; Blumenthal, James A. PhD; Kuhn, Cynthia M. PhD; Sherwood, Andrew PhD

doi: 10.1097/PSY.0000000000000144

Objective Depression and anxiety are considered risk factors for cardiovascular disease (CVD). The explanatory mechanisms, however, are still to be characterized. One proposed pathophysiological pathway is dysregulation of the autonomic nervous system, including heightened sympathetic nervous system activity. This study examined the relationship between symptoms of depression, anxiety, and sympathetic nervous system activity in individuals with untreated high blood pressure.

Methods A total of 140 participants with untreated high blood pressure (55% white, 38.5% female, mean [standard deviation] age = 45.5 [8.55] years) collected urine over a 24-hour period on 3 separate occasions. Urine samples were assayed for mean 24-hour epinephrine (EPI24) and norepinephrine excretion. Depressive symptoms were assessed using the Beck Depression Inventory, with anxiety symptoms assessed using the Spielberger State-Trait Anxiety Inventory.

Results Depression and anxiety scores were intercorrelated (r = 0.76, p < .001). EPI24 was positively correlated with anxiety (r = 0.20, p = .02) but not depression (r = 0.02, p = .77), whereas 24-hour urinary norepinephrine excretion was not correlated with anxiety (r = 0.10, p = .21) or with depression (r = 0.07, p = .39). Regression models, accounting for sex, age, body mass index, race, mean systolic ambulatory blood pressure, tobacco use, alcohol use, physical activity, and sleep efficiency confirmed that anxiety was associated with EPI24 excretion (p = .023) and that depressive symptoms were not (p = .54).

Conclusions Anxiety was associated with heightened sympathoadrenal activity, suggesting a biological pathway through which anxiety could increase CVD risk. Anxiety and depression may confer increased CVD risk via different mechanisms.

Supplemental digital content is available in the text.

From the Department of Psychiatry and Behavioral Sciences (Paine, Watkins, Blumenthal, Kuhn, Sherwood) and Pharmacology and Cancer Biology (Kuhn), Duke University Medical Center, Durham, North Carolina.

Supplemental Content

Address correspondence and reprint requests to Andrew Sherwood, PhD, Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Box 3119, Durham, NC 27710. E-mail:

Received for publication April 23, 2014; revision received October 25, 2014.

Copyright © 2015 by American Psychosomatic Society
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