@article{ isingrini_fluoxetine_2012,
  title = {Fluoxetine effect on aortic nitric oxide-dependent vasorelaxation in the unpredictable chronic mild stress model of depression in mice},
  volume = {74},
  issn = {1534-7796},
  doi = {10.1097/PSY.0b013e31823a43e0},
  abstract = {{OBJECTIVE}: Major depression is an independent risk factor for the development of cardiovascular diseases. However, the exact mechanism by which depression may induce cardiovascular events is unclear. Endothelial dysfunction has been reported as a possible link between depression and subsequent cardiovascular events as described in depressed subjects. The purpose of this study was to investigate endothelial dysfunction and atherosclerosis formation in the aorta of mice exposed to the unpredictable chronic mild stress ({UCMS}) procedure.
{METHODS}: {BALB}/c mice were exposed to two 7-week {UCMS} procedures separated by 6 weeks. Treatments (fluoxetine 10 mg/kg; {NaCl} 0.9%) started at the third week until the end of the seventh week of each procedure. Endothelial function was evaluated by in vitro assessment of acetylcholine-induced vasorelaxation in aortic rings. By using specific inhibitors for nitric oxide ({NO})- and prostacyclin-dependent relaxation, we assessed the part played by {NO}, prostacyclin, and endothelium-derived hyperpolarizing factor ({EDHF})-like mediators in endothelium-dependent relaxation. Atherosclerosis was evaluated by histological examination.
{RESULTS}: Depression-like behavior was increased in the {UCMS} versus unstressed group and was reversed by chronic fluoxetine treatment. Vascular reactivity study indicated that {UCMS} induced a decrease in the {NO}-dependent relaxation that was partially compensated by an {EDHF}-like dependent relaxation. Because fluoxetine per se increased the {NO}-dependent relaxation, fluoxetine was able to reverse {UCMS} effect on the {NO} component and abolished the {EDHF}-like component. Atherosclerotic lesion was found in aorta of {UCMS} and nonstressed animals.
{CONCLUSIONS}: As an independent risk factor, {UCMS} reproduced the endothelial alterations observed in depression but was not sufficient to provoke morphological alterations.},
  language = {eng},
  number = {1},
  journal = {Psychosomatic Medicine},
  author = {Isingrini, Elsa and Belzung, Catherine and Freslon, Jean-Louis and Machet, Marie-Christine and Camus, Vincent},
  month = {January},
  year = {2012},
  pmid = {22210237},
  keywords = {Acetylcholine, Animals, Aorta, Atherosclerosis, Biological Factors, Depressive Disorder, Major, Disease Models, Animal, Dose-Response Relationship, Drug, Endothelium, Vascular, Endothelium-Dependent Relaxing Factors, Epoprostenol, Fluoxetine, Logistic Models, Mice, Mice, Inbred {BALB} C, Nitric Oxide, Random Allocation, Serotonin Uptake Inhibitors, Stress, Psychological, Vasodilation},
  pages = {63--72}
}

{"_id":"AuHjifx9YqTmGD6eK","authorIDs":[],"author_short":["Isingrini, E.","Belzung, C.","Freslon, J.","Machet, M.C.","Camus, V."],"bibbaseid":"isingrini-belzung-freslon-machet-camus-fluoxetineeffectonaorticnitricoxidedependentvasorelaxationintheunpredictablechronicmildstressmodelofdepressioninmice-2012","bibdata":{"abstract":"OBJECTIVE: Major depression is an independent risk factor for the development of cardiovascular diseases. However, the exact mechanism by which depression may induce cardiovascular events is unclear. Endothelial dysfunction has been reported as a possible link between depression and subsequent cardiovascular events as described in depressed subjects. The purpose of this study was to investigate endothelial dysfunction and atherosclerosis formation in the aorta of mice exposed to the unpredictable chronic mild stress (UCMS) procedure. METHODS: BALB/c mice were exposed to two 7-week UCMS procedures separated by 6 weeks. Treatments (fluoxetine 10 mg/kg; NaCl 0.9%) started at the third week until the end of the seventh week of each procedure. Endothelial function was evaluated by in vitro assessment of acetylcholine-induced vasorelaxation in aortic rings. By using specific inhibitors for nitric oxide (NO)- and prostacyclin-dependent relaxation, we assessed the part played by NO, prostacyclin, and endothelium-derived hyperpolarizing factor (EDHF)-like mediators in endothelium-dependent relaxation. Atherosclerosis was evaluated by histological examination. RESULTS: Depression-like behavior was increased in the UCMS versus unstressed group and was reversed by chronic fluoxetine treatment. Vascular reactivity study indicated that UCMS induced a decrease in the NO-dependent relaxation that was partially compensated by an EDHF-like dependent relaxation. Because fluoxetine per se increased the NO-dependent relaxation, fluoxetine was able to reverse UCMS effect on the NO component and abolished the EDHF-like component. Atherosclerotic lesion was found in aorta of UCMS and nonstressed animals. CONCLUSIONS: As an independent risk factor, UCMS reproduced the endothelial alterations observed in depression but was not sufficient to provoke morphological alterations.","author":["Isingrini, Elsa","Belzung, Catherine","Freslon, Jean-Louis","Machet, Marie-Christine","Camus, Vincent"],"author_short":["Isingrini, E.","Belzung, C.","Freslon, J.","Machet, M.C.","Camus, V."],"bibtex":"@article{ isingrini_fluoxetine_2012,\n title = {Fluoxetine effect on aortic nitric oxide-dependent vasorelaxation in the unpredictable chronic mild stress model of depression in mice},\n volume = {74},\n issn = {1534-7796},\n doi = {10.1097/PSY.0b013e31823a43e0},\n abstract = {{OBJECTIVE}: Major depression is an independent risk factor for the development of cardiovascular diseases. However, the exact mechanism by which depression may induce cardiovascular events is unclear. Endothelial dysfunction has been reported as a possible link between depression and subsequent cardiovascular events as described in depressed subjects. The purpose of this study was to investigate endothelial dysfunction and atherosclerosis formation in the aorta of mice exposed to the unpredictable chronic mild stress ({UCMS}) procedure.\n{METHODS}: {BALB}/c mice were exposed to two 7-week {UCMS} procedures separated by 6 weeks. Treatments (fluoxetine 10 mg/kg; {NaCl} 0.9%) started at the third week until the end of the seventh week of each procedure. Endothelial function was evaluated by in vitro assessment of acetylcholine-induced vasorelaxation in aortic rings. By using specific inhibitors for nitric oxide ({NO})- and prostacyclin-dependent relaxation, we assessed the part played by {NO}, prostacyclin, and endothelium-derived hyperpolarizing factor ({EDHF})-like mediators in endothelium-dependent relaxation. Atherosclerosis was evaluated by histological examination.\n{RESULTS}: Depression-like behavior was increased in the {UCMS} versus unstressed group and was reversed by chronic fluoxetine treatment. Vascular reactivity study indicated that {UCMS} induced a decrease in the {NO}-dependent relaxation that was partially compensated by an {EDHF}-like dependent relaxation. Because fluoxetine per se increased the {NO}-dependent relaxation, fluoxetine was able to reverse {UCMS} effect on the {NO} component and abolished the {EDHF}-like component. Atherosclerotic lesion was found in aorta of {UCMS} and nonstressed animals.\n{CONCLUSIONS}: As an independent risk factor, {UCMS} reproduced the endothelial alterations observed in depression but was not sufficient to provoke morphological alterations.},\n language = {eng},\n number = {1},\n journal = {Psychosomatic Medicine},\n author = {Isingrini, Elsa and Belzung, Catherine and Freslon, Jean-Louis and Machet, Marie-Christine and Camus, Vincent},\n month = {January},\n year = {2012},\n pmid = {22210237},\n keywords = {Acetylcholine, Animals, Aorta, Atherosclerosis, Biological Factors, Depressive Disorder, Major, Disease Models, Animal, Dose-Response Relationship, Drug, Endothelium, Vascular, Endothelium-Dependent Relaxing Factors, Epoprostenol, Fluoxetine, Logistic Models, Mice, Mice, Inbred {BALB} C, Nitric Oxide, Random Allocation, Serotonin Uptake Inhibitors, Stress, Psychological, Vasodilation},\n pages = {63--72}\n}","bibtype":"article","doi":"10.1097/PSY.0b013e31823a43e0","id":"isingrini_fluoxetine_2012","issn":"1534-7796","journal":"Psychosomatic Medicine","key":"isingrini_fluoxetine_2012","keywords":"Acetylcholine, Animals, Aorta, Atherosclerosis, Biological Factors, Depressive Disorder, Major, Disease Models, Animal, Dose-Response Relationship, Drug, Endothelium, Vascular, Endothelium-Dependent Relaxing Factors, Epoprostenol, Fluoxetine, Logistic Models, Mice, Mice, Inbred BALB C, Nitric Oxide, Random Allocation, Serotonin Uptake Inhibitors, Stress, Psychological, Vasodilation","language":"eng","month":"January","number":"1","pages":"63--72","pmid":"22210237","title":"Fluoxetine effect on aortic nitric oxide-dependent vasorelaxation in the unpredictable chronic mild stress model of depression in mice","type":"article","volume":"74","year":"2012","bibbaseid":"isingrini-belzung-freslon-machet-camus-fluoxetineeffectonaorticnitricoxidedependentvasorelaxationintheunpredictablechronicmildstressmodelofdepressioninmice-2012","role":"author","urls":{},"keyword":["Acetylcholine","Animals","Aorta","Atherosclerosis","Biological Factors","Depressive Disorder","Major","Disease Models","Animal","Dose-Response Relationship","Drug","Endothelium","Vascular","Endothelium-Dependent Relaxing Factors","Epoprostenol","Fluoxetine","Logistic Models","Mice","Mice","Inbred BALB C","Nitric Oxide","Random Allocation","Serotonin Uptake Inhibitors","Stress","Psychological","Vasodilation"],"downloads":0},"bibtype":"article","biburl":"https://api.zotero.org/users/1159944/collections/PSAWXGQV/items?key=8pKJLEr2Uh7GZN5GrRPdT9lZ&format=bibtex&limit=100","creationDate":"2015-02-11T08:36:06.141Z","downloads":0,"keywords":["acetylcholine","animals","aorta","atherosclerosis","biological factors","depressive disorder","major","disease models","animal","dose-response relationship","drug","endothelium","vascular","endothelium-dependent relaxing factors","epoprostenol","fluoxetine","logistic models","mice","mice","inbred balb c","nitric oxide","random allocation","serotonin uptake inhibitors","stress","psychological","vasodilation"],"search_terms":["fluoxetine","effect","aortic","nitric","oxide","dependent","vasorelaxation","unpredictable","chronic","mild","stress","model","depression","mice","isingrini","belzung","freslon","machet","camus"],"title":"Fluoxetine effect on aortic nitric oxide-dependent vasorelaxation in the unpredictable chronic mild stress model of depression in mice","year":2012,"dataSources":["FRxCKR7bxZrk5oFSo"]}