Chronic selective serotonin reuptake inhibition modulates endothelial dysfunction and oxidative state in rat chronic mild stress model of depression

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Chronic selective serotonin reuptake inhibition modulates endothelial dysfunction and oxidative state in rat chronic mild stress model of depression. / Matchkov, V.V.; Kravtsova, V.V.; Wiborg, O.; Aalkjaer, C.; Bouzinova, E.V.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 309, No. 8, 2015, p. R814-R823.

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Author

Matchkov, V.V. ; Kravtsova, V.V. ; Wiborg, O. ; Aalkjaer, C. ; Bouzinova, E.V. / Chronic selective serotonin reuptake inhibition modulates endothelial dysfunction and oxidative state in rat chronic mild stress model of depression. In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology. 2015 ; Vol. 309, No. 8. pp. R814-R823.

BibTeX

@article{1862a39d09b94978b0f27d2c8385d04b,

title = "Chronic selective serotonin reuptake inhibition modulates endothelial dysfunction and oxidative state in rat chronic mild stress model of depression",

abstract = "Major depression is known to be associated with cardiovascular abnormalities and oxidative stress has been suggested to play a role. We tested the hypothesis that antidepressant treatment reduces oxidative stress, and endothelial dysfunctions in the chronic mild stress (CMS) model of depression in rats. Rats with >30% reduction in sucrose intake after 4 weeks of CMS were defined in the study as CMS-susceptible and compared to unstressed controls. Sixteen CMS-susceptible and 8 unstressed rats were treated during weeks 5 to 8 of the CMS protocol with escitalopram. Escitalopram-treated rats with >20% recovery in the sucrose consumption during the last 2 weeks of treatment were defined as escitalopram responders. Rats which did not reach these criteria were defined as escitalopram non-responders. In the open field test escitalopram responders demonstrated anxiolytic effect of treatment. In mesenteric small arteries escitalopram affected neither NO nor COX-1 mediated vasodilation. Escitalopram potentiated endothel",

keywords = "chronic mild stress, depression, endothelium, escitalopram, oxidative stress",

author = "V.V. Matchkov and V.V. Kravtsova and O. Wiborg and C. Aalkjaer and E.V. Bouzinova",

year = "2015",

doi = "10.1152/ajpregu.00337.2014",

language = "English",

volume = "309",

pages = "R814--R823",

journal = "American Journal of Physiology - Regulatory Integrative and Comparative Physiology",

issn = "0363-6119",

publisher = "American Physiological Society",

number = "8",

}

RIS

TY - JOUR

T1 - Chronic selective serotonin reuptake inhibition modulates endothelial dysfunction and oxidative state in rat chronic mild stress model of depression

AU - Matchkov, V.V.

AU - Kravtsova, V.V.

AU - Wiborg, O.

AU - Aalkjaer, C.

AU - Bouzinova, E.V.

PY - 2015

Y1 - 2015

N2 - Major depression is known to be associated with cardiovascular abnormalities and oxidative stress has been suggested to play a role. We tested the hypothesis that antidepressant treatment reduces oxidative stress, and endothelial dysfunctions in the chronic mild stress (CMS) model of depression in rats. Rats with >30% reduction in sucrose intake after 4 weeks of CMS were defined in the study as CMS-susceptible and compared to unstressed controls. Sixteen CMS-susceptible and 8 unstressed rats were treated during weeks 5 to 8 of the CMS protocol with escitalopram. Escitalopram-treated rats with >20% recovery in the sucrose consumption during the last 2 weeks of treatment were defined as escitalopram responders. Rats which did not reach these criteria were defined as escitalopram non-responders. In the open field test escitalopram responders demonstrated anxiolytic effect of treatment. In mesenteric small arteries escitalopram affected neither NO nor COX-1 mediated vasodilation. Escitalopram potentiated endothel

AB - Major depression is known to be associated with cardiovascular abnormalities and oxidative stress has been suggested to play a role. We tested the hypothesis that antidepressant treatment reduces oxidative stress, and endothelial dysfunctions in the chronic mild stress (CMS) model of depression in rats. Rats with >30% reduction in sucrose intake after 4 weeks of CMS were defined in the study as CMS-susceptible and compared to unstressed controls. Sixteen CMS-susceptible and 8 unstressed rats were treated during weeks 5 to 8 of the CMS protocol with escitalopram. Escitalopram-treated rats with >20% recovery in the sucrose consumption during the last 2 weeks of treatment were defined as escitalopram responders. Rats which did not reach these criteria were defined as escitalopram non-responders. In the open field test escitalopram responders demonstrated anxiolytic effect of treatment. In mesenteric small arteries escitalopram affected neither NO nor COX-1 mediated vasodilation. Escitalopram potentiated endothel

KW - chronic mild stress

KW - depression

KW - endothelium

KW - escitalopram

KW - oxidative stress

U2 - 10.1152/ajpregu.00337.2014

DO - 10.1152/ajpregu.00337.2014

M3 - Article

VL - 309

SP - R814-R823

JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology

JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology

SN - 0363-6119

IS - 8

ER -

ID: 3943651