Abstract:Objective-There is a bidirectional relationship between mood disorders (e.g., depression) and altered cardiovascular regulation (e.g., heart disease), however the precise causal and/or common mechanisms underlying this association are unclear. In previous studies we have noted indications of altered sympathetic drive to the heart in rats that exhibit anhedonia, an operational sign of depression induced by subjecting the animals to a series of mild and unpredictable stressors [chronic mild stress (CMS) rodent m… Show more
“…Some cardiovascular changes are reported for the CMS model, e.g., elevated heart rate and reduced heart rate variability associated with changes in the sympathetic/parasympathetic balance (26,27,29). Moreover, although anhedonia disappears following cessation of the stressors, the cardiovascular changes persist for some time, suggesting that they are firmly established (26,28).…”
Matchkov VV, Kravtsova VV, Wiborg O, Aalkjaer C, Bouzinova EV. Chronic selective serotonin reuptake inhibition modulates endothelial dysfunction and oxidative state in rat chronic mild stress model of depression. Am J Physiol Regul Integr Comp Physiol 309: R814 -R823, 2015. First published August 12, 2015 doi:10.1152/ajpregu.00337.2014.-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 Ͼ30% reduction in sucrose intake after 4 wk of CMS were defined in the study as CMS-susceptible and compared with unstressed controls. Sixteen CMS-susceptible and eight unstressed rats were treated during weeks 5 to 8 of the CMS protocol with escitalopram. Escitalopram-treated rats with Ͼ20% recovery in the sucrose consumption during the last 2 wk of treatment were defined as escitalopram responders. Rats that did not reach these criteria were defined as escitalopram nonresponders. In the open field test, escitalopram responders demonstrated anxiolytic effect of treatment. In mesenteric small arteries, escitalopram affected neither NO nor cyclooxygenase-1 (COX-1)-mediated vasodilation. Escitalopram potentiated endothelium-dependent hyperpolarization-like response, which was suppressed in the vehicle-treated CMS-susceptible rats and reduced COX-2-dependent relaxation, which was elevated in the vehicle-treated CMS-susceptible rats. Escitalopram did not affect blood pressure and heart rate, which were elevated in the vehicle-treated CMS-susceptible rats. Oxidative stress markers were changed in association with CMS in liver, heart, and brain. Escitalopram normalized oxidative stress markers in the majority of tissues. This study demonstrates that the antidepressant effect of escitalopram is associated with partial improvement of endothelial function in small arteries affecting COX-2 and endothelium-dependent hyperpolarization-like pathways.depression; chronic mild stress; escitalopram; endothelium; nitric oxide synthase; cyclooxygenase; endothelium-derived hyperpolarization; oxidative stress; glutathione; malondialdehyde CARDIOVASCULAR DISEASES AND major depressive disorder are the two most prevalent health problems in high-income countries (31). Their comorbidity is well recognized, but the mechanisms and critical factors underlying this comorbidity are unknown. Interactions between several factors common for both disorders are complex (17; 43). Thus, a dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis and activation of the renin-angiotensin-aldosterone system lead to changes associated with both depression and cardiovascular abnormalities.Also dysfunction of the autonomic nervous system (sympathetic/parasympathetic) is known to be involved, as well as an activation of proinflammatory cytokines (46). Importantly, these factors can induce both depression and ch...
“…Some cardiovascular changes are reported for the CMS model, e.g., elevated heart rate and reduced heart rate variability associated with changes in the sympathetic/parasympathetic balance (26,27,29). Moreover, although anhedonia disappears following cessation of the stressors, the cardiovascular changes persist for some time, suggesting that they are firmly established (26,28).…”
Matchkov VV, Kravtsova VV, Wiborg O, Aalkjaer C, Bouzinova EV. Chronic selective serotonin reuptake inhibition modulates endothelial dysfunction and oxidative state in rat chronic mild stress model of depression. Am J Physiol Regul Integr Comp Physiol 309: R814 -R823, 2015. First published August 12, 2015 doi:10.1152/ajpregu.00337.2014.-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 Ͼ30% reduction in sucrose intake after 4 wk of CMS were defined in the study as CMS-susceptible and compared with unstressed controls. Sixteen CMS-susceptible and eight unstressed rats were treated during weeks 5 to 8 of the CMS protocol with escitalopram. Escitalopram-treated rats with Ͼ20% recovery in the sucrose consumption during the last 2 wk of treatment were defined as escitalopram responders. Rats that did not reach these criteria were defined as escitalopram nonresponders. In the open field test, escitalopram responders demonstrated anxiolytic effect of treatment. In mesenteric small arteries, escitalopram affected neither NO nor cyclooxygenase-1 (COX-1)-mediated vasodilation. Escitalopram potentiated endothelium-dependent hyperpolarization-like response, which was suppressed in the vehicle-treated CMS-susceptible rats and reduced COX-2-dependent relaxation, which was elevated in the vehicle-treated CMS-susceptible rats. Escitalopram did not affect blood pressure and heart rate, which were elevated in the vehicle-treated CMS-susceptible rats. Oxidative stress markers were changed in association with CMS in liver, heart, and brain. Escitalopram normalized oxidative stress markers in the majority of tissues. This study demonstrates that the antidepressant effect of escitalopram is associated with partial improvement of endothelial function in small arteries affecting COX-2 and endothelium-dependent hyperpolarization-like pathways.depression; chronic mild stress; escitalopram; endothelium; nitric oxide synthase; cyclooxygenase; endothelium-derived hyperpolarization; oxidative stress; glutathione; malondialdehyde CARDIOVASCULAR DISEASES AND major depressive disorder are the two most prevalent health problems in high-income countries (31). Their comorbidity is well recognized, but the mechanisms and critical factors underlying this comorbidity are unknown. Interactions between several factors common for both disorders are complex (17; 43). Thus, a dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis and activation of the renin-angiotensin-aldosterone system lead to changes associated with both depression and cardiovascular abnormalities.Also dysfunction of the autonomic nervous system (sympathetic/parasympathetic) is known to be involved, as well as an activation of proinflammatory cytokines (46). Importantly, these factors can induce both depression and ch...
“…Sendo assim, sabe-se que a ligação entre a depressão e a alterações cardiovasculares pode ser mediada em parte por mecanismos autônomos que contribuem para a regularização da função cardiovascular (Grippo et al, 2008).…”
Section: Sumáriounclassified
“…Além disso, Grippo et al, (2008) demonstraram que ratos adultos expostos ao ECV apresentaram redução na resposta do barorreflexo induzida por diminuição da pressão arterial.…”
Section: Sumáriounclassified
“…Além dessas alterações no peso e comportamento, vários estudos demonstram que o estresse pode levar a alterações no sistema circulatório, dependendo do tipo de estressor envolvido (Esch et al, 2002), uma vez que a exposição ao estresse provoca o aumento da PA e da FC (Irvine et al, 1997, Barres et al, 2004, Carrive, 2006, Tavares and Correa, 2006, Grippo et al, 2008, Duarte et al, 2015b. Nossos achados estão em conformidade com estudos de Grippo et al, (2006) Embora as alterações cardiovasculares sejam comuns frente à exposição ao estresse, elas podem variar de acordo com os diferentes estressores utilizados (Crestani et al, 2010c).…”
Section: Figura 38 (Ab)unclassified
“…(Crestani et al, 2010c). Devido a isto, vários estudos realizados em humanos e animais têm apontado associação entre estresse, arritmias cardíacas e hipertensão (Grippo et al, 2002(Grippo et al, , 2008 e sugerem que estressores ambientais podem influenciar a regulação autonômica e patogênese das doenças cardiovasculares (Carpeggiani and Skinner, 1991). Sendo assim, vários estudos em modelos animais propõem que as alterações fisiológicas decorrentes à exposição ao estresse dependem de fatores tais como tipo do estresse, duração, frequência e intensidade do estímulo aversivo ao qual o animal é submetido (Natelson et al, 1988, Aguilera, 1998, Jankord and Herman, 2008.…”
Efeitos do estresse crônico sobre as respostas cardiovasculares e ventilatórias ativadas pelo quimiorreflexo e barorreflexo em ratos
LISTA DE ABREVIATURAS
ABSTRACT
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ABSTRACTThe body is submitted to various stressful stimuli that may affect many physiological processes. Although blood pressure and heart rate oscilations are common during exposure to stress, they can vary according to the different stressors type, duration, frequency and intensity of the aversive stimulus.
Interaction between the autonomic nervous system and the neuroendocrine system is critical for maintenance of homeostasis in a wide variety of physiological parameters such as body temperature, fluid and electrolyte balance, and blood pressure and volume. The anatomical and physiological mechanisms underlying integration of the neuroendocrine and autonomic mechanisms responsible for eliciting integrated autonomic and neuroendocrine actions are the focus of this article. This includes a focus on the hypothalamic paraventricular nucleus, because it includes both neuroendocrine neurons and preganglionic autonomic neurons that regulate sympathetic and parasympathetic outflow. The "wired" and "nonwired" mechanisms within PVN that facilitate communication between these neuronal populations are described. The impact of peripheral hormones, specifically the adrenal and gonadal steroids, on the neuroendocrine and autonomic systems is discussed, and exercise is used as a specific example of a physiological challenge/stress that requires precise integration of neuroendocrine and autonomic responses to maintain cardiovascular, fluid, and energy homeostasis.
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