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Social isolation causes endothelial dysfunction: implications for depression and cardiovascular disease
Author(s) -
Grippo Angela J,
Peuler Jacob D,
Phelps Laura E,
Scotti Melissa-Ann L,
McNeal Neal
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1091.20
Subject(s) - social isolation , acetylcholine , prairie vole , medicine , endothelial dysfunction , endothelium , endocrinology , relaxation (psychology) , depression (economics) , isolation (microbiology) , cardiology , biology , bioinformatics , psychiatry , ecology , macroeconomics , economics , microtus
Humans with depression show endothelial dysfunction, one recent demonstration of which was reduced acetylcholine (ACh)‐induced relaxation of adrenergically‐precontracted small arteries biopsied from depressed patients. Accordingly, we examined vascular reactivity to ACh in the socially isolated prairie vole, an animal model relevant to depression. Thoracic aortas were removed from female prairie voles after 4 weeks of social isolation (vs pairing with a sibling). ACh‐induced relaxations were notably reduced by social isolation with maximum relaxation reaching only 30% of adrenergic precontraction (compared to 47% in aortas from paired controls). Removal of endothelium from an additional set of aortic tissues abolished all ACh relaxations including the difference between paired and isolated groups. In these same tissues the nitric oxide (NO)‐donor nitroprusside completely relaxed all precontractions of the smooth muscle, unaltered by isolation. Thus, social isolation of the prairie vole may impair release of protective relaxing factors like NO from vascular endothelium without altering smooth muscle responsiveness to them. This is the first animal model of depression due solely to chronic isolation to show this phenomenon. These findings provide insight into the role of the social environment in mediating the association of depression and cardiovascular disease. Support: MH77581, NIU, MWU.