Journal
STRESS-THE INTERNATIONAL JOURNAL ON THE BIOLOGY OF STRESS
Volume 12, Issue 1, Pages 1-21Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/10253890802046281
Keywords
Baroreceptor reflex; chronic fatigue; chronic mild stress; congestive heart failure; cytokine; heart rate variability
Funding
- United States Public Health Service [DK-66086, GM-07069, HL-14388, HL-57472, HL-63915, MH-58448, MH-65839, MH-73233, MH-77581, NS-34154]
- National Center for Research Resources [S10RR016652]
- NATIONAL CENTER FOR RESEARCH RESOURCES [S10RR016652] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [T32HL007121, R01HL063915, R01HL057472, P01HL014388] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK066086] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007069] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [R21MH077581, F31MH065839, R01MH058448, F32MH073233] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS034154, R01NS034153] Funding Source: NIH RePORTER
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Bidirectional associations between mood disorders and cardiovascular diseases are extensively documented. However, the precise physiological and biochemical mechanisms that underlie such relationships are not well understood. This review focuses on the neurobiological processes and mediators that are common to both mood and cardiovascular disorders. The discussion places an emphasis on the role of exogenous stressors in addition to: (a) neuroendocrine and neurohumoral changes involving dysfunction of the hypothalamic-pituitary-adrenal axis and the activation of the renin-angiotensin-aldosterone system, (b) immune alterations including activation of pro-inflammatory cytokines, (c) autonomic and cardiovascular dysregulation including increased sympathetic drive, withdrawal of parasympathetic tone, cardiac rate and rhythm disturbances, and altered baroreceptor reflex function, (d) central neurotransmitter system dysfunction involving the dopamine, norepinephrine and serotonin systems, and (e) behavioral changes including fatigue and physical inactivity. The review also discusses experimental investigations using preclinical disease models to elucidate the neurobiological mechanisms underlying the link between mood disorders and cardiovascular disease. These include: (a) the chronic mild stress model of depression, (b) a model of congestive heart failure, (c) a model of cardiovascular deconditioning, (d) pharmacological manipulations of body fluid and sodium balance, and (e) pharmacological manipulations of the central serotonergic system. In combination with an extensive human research literature, the investigation of mechanisms underlying mood and cardiovascular regulation using animal models will enhance understanding the association between depression and cardiovascular disease. This will ultimately promote the development of better treatments and interventions for individuals with co-morbid psychological and somatic pathologies.
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