Stress, depression and cardiovascular dysregulation: a review of neurobiological mechanisms and the integration of research from preclinical disease models

Angela J Grippo; Alan Kim Johnson

doi:10.1080/10253890802046281

Back

Stress, depression and cardiovascular dysregulation: a review of neurobiological mechanisms and the integration of research from preclinical disease models

Journal article

Peer reviewed

Stress, depression and cardiovascular dysregulation: a review of neurobiological mechanisms and the integration of research from preclinical disease models

Angela J Grippo and Alan Kim Johnson

Stress (Amsterdam, Netherlands), Vol.12(1), pp.1-21

01/2009

DOI: 10.1080/10253890802046281

PMCID: PMC2613299

PMID: 19116888

Files and links (1)

url

https://www.ncbi.nlm.nih.gov/pmc/articles/2613299View

Open Access

Abstract

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.

Animals

Autonomic Nervous System - physiopathology

Baroreflex

Cardiovascular Diseases - physiopathology

Cardiovascular System - physiopathology

Cytokines - physiology

Depression - complications

Depression - physiopathology

Disease Models, Animal

Fatigue - complications

Humans

Hypothalamo-Hypophyseal System - physiopathology

Mood Disorders - physiopathology

Pituitary-Adrenal System - physiopathology

Renin-Angiotensin System - physiology

Serotonin - physiology

Stress, Psychological - physiopathology

Details

Title: Subtitle: Stress, depression and cardiovascular dysregulation: a review of neurobiological mechanisms and the integration of research from preclinical disease models
Creators: Angela J Grippo - Department of Psychiatry and Brain Body Center, University of Illinois at Chicago, Chicago, IL 60612, USA. agrippo@psych.uic.edu
Alan Kim Johnson
Resource Type: Journal article
Publication Details: Stress (Amsterdam, Netherlands), Vol.12(1), pp.1-21
DOI: 10.1080/10253890802046281
PMID: 19116888
PMCID: PMC2613299
NLM abbreviation: Stress
ISSN: 1025-3890
eISSN: 1607-8888
Grant note: R01 DK066086 / NIDDK NIH HHS F32 MH073233-02 / NIMH NIH HHS MH-65839 / NIMH NIH HHS R01 HL063915-05 / NHLBI NIH HHS T32 GM007069 / NIGMS NIH HHS F31 MH065839-02 / NIMH NIH HHS F32 MH073233 / NIMH NIH HHS R01 HL063915 / NHLBI NIH HHS P01 HL014388 / NHLBI NIH HHS F32 MH073233-01 / NIMH NIH HHS HL-57472 / NHLBI NIH HHS R01 HL057472 / NHLBI NIH HHS R21 MH077581-01A2 / NIMH NIH HHS F31 MH065839-01 / NIMH NIH HHS HL-63915 / NHLBI NIH HHS R21 MH077581 / NIMH NIH HHS MH-58448 / NIMH NIH HHS S10 RR016652-01 / NCRR NIH HHS MH-77581 / NIMH NIH HHS NS-34154 / NINDS NIH HHS R01 MH058448 / NIMH NIH HHS F31 MH065839 / NIMH NIH HHS R01 HL057472-09 / NHLBI NIH HHS HL-14388 / NHLBI NIH HHS R01 MH058448-04 / NIMH NIH HHS P01 HL014388-35 / NHLBI NIH HHS R01 NS034153-07 / NINDS NIH HHS GM-07069 / NIGMS NIH HHS F32 MH073233-03 / NIMH NIH HHS T32 HL007121 / NHLBI NIH HHS S10RR016652 / NCRR NIH HHS T32 GM007069-25 / NIGMS NIH HHS DK-66086 / NIDDK NIH HHS MH-73233 / NIMH NIH HHS R01 MH058448-05 / NIMH NIH HHS
Language: English
Date published: 01/2009
Academic Unit: Psychological and Brain Sciences; Neuroscience and Pharmacology; Health, Sport, and Human Physiology
Record Identifier: 9984213429802771

Metrics

23 Record Views

337 Times Cited - Web of Science