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Am J Physiol Regul Integr Comp Physiol (January 24, 2002). doi:10.1152/ajpregu.00614.2001
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Articles in PresS, published online ahead of print January 24, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00614.2001
Submitted on October 10, 2001
Accepted on January 2, 2002

Cardiovascular Alterations and Autonomic Imbalance in an Experimental Model of Depression

Angela J Grippo1, Julia A Moffitt2, and Alan K Johnson3*

1 Department of Psychology, University of Iowa, Iowa City, IA, USA; Department of Cardiovascular Center, University of Iowa, Iowa City, IA, USA
2 Department of Cardiovascular Center, University of Iowa, Iowa City, IA, USA
3 Department of Psychology, University of Iowa, Iowa City, IA, USA; Department of Pharmacology, University of Iowa, Iowa City, IA, USA; Department of Cardiovascular Center, University of Iowa, Iowa City, IA, USA

* To whom correspondence should be addressed. E-mail: alan-johnson{at}uiowa.edu.

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 weeks 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.




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