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Am J Physiol Regul Integr Comp Physiol 282: R1333-R1341, 2002. First published January 24, 2002; doi:10.1152/ajpregu.00614.2001
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Vol. 282, Issue 5, R1333-R1341, May 2002

Cardiovascular alterations and autonomic imbalance in an experimental model of depression

Angela J. Grippo1,2, Julia A. Moffitt2, and Alan Kim Johnson1,2,3,4

Departments of 1 Psychology, 4 Pharmacology, and 3 Exercise Science, and 2 The Cardiovascular Center, University of Iowa, Iowa City, Iowa 52242

Depressed patients with and without a history of cardiovascular pathology display signs, such as elevated heart rate, decreased heart rate variability, and increased physiological reactivity to environmental stressors, which may indicate a predisposition to cardiovascular disease. The specific physiological mechanisms associating depression with such altered cardiovascular parameters are presently unclear. The current study investigated cardiovascular regulation in the chronic mild stress rodent model of depression and examined the specific autonomic nervous system mechanisms underlying the responses. Sprague-Dawley rats exposed to a series of mild, unpredictable stressors over 4 wk displayed anhedonia (an essential feature of human depression), along with elevated resting heart rate, decreased heart rate variability, and exaggerated pressor and heart rate responses to air jet stress. Results obtained from experiments studying autonomic blockade suggest that cardiovascular alterations in the chronic mild stress model are mediated by elevated sympathetic tone to the heart. The present findings have implications for the study of pathophysiological links between affective disorders and cardiovascular disease.

autonomic blockade; cardiovascular disease; chronic mild stress; heart rate variability


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