Adolescent vulnerability to cardiovascular consequences of chronic emotional stress: Review and perspectives for future research

Crestani, Carlos C.

doi:10.1016/j.neubiorev.2016.03.027

Cited by 17 publications

(13 citation statements)

References 113 publications

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“…Convergent clinical and preclinical studies have provided evidence that emotional stress is a modifiable risk factor for several cardiovascular dysfunctions (Sgoifo et al , ; Cohen et al , ; Crestani, ). Substances that modulate endocannabinoid neurotransmission have been indicated as a promising strategy for the treatment of cardiovascular dysfunctions (Carnevali et al , ).…”

Section: Discussionmentioning

confidence: 99%

Involvement of endocannabinoid neurotransmission in the bed nucleus of stria terminalis in cardiovascular responses to acute restraint stress in rats

Gomes‐de‐Souza

Oliveira

Benini

et al. 2016

British J Pharmacology

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Graduate Program in Physiological Sciences, São Carlos, SP, Brazil BACKGROUND AND PURPOSEEndocannabinoid signalling has been reported as an important neurochemical mechanism involved in responses to stress. Previous studies provided evidence of endocannabinoid release in the bed nucleus of the stria terminalis (BNST) during aversive stimuli. Nevertheless, a possible involvement of this neurochemical mechanism in stress responses has never been evaluated. Therefore, in the present study we investigated the involvement of BNST endocannabinoid neurotransmission, acting via local CB 1 receptors, in the cardiovascular responses to acute restraint stress in rats. EXPERIMENTAL APPROACHThe selective CB 1 receptor antagonist AM251 (1, 30 and 100 pmol 100 nL À1 ) and/or the fatty acid amide hydrolase (FAAH) enzyme inhibitor URB597 (30 pmol 100 nL À1 ) or the monoacylglycerol lipase (MAGL) enzyme inhibitor JZL184 (30 pmol 100 nL À1 ) was microinjected into the BNST before the acute restraint stress. KEY RESULTSMicroinjection of AM251 into the BNST enhanced the tachycardia caused by restraint stress, without affecting the increase in arterial pressure and the sympathetic-mediated cutaneous vasoconstrictor response. Conversely, the increased endogenous levels of AEA in the BNST evoked by local treatment with the FAAH enzyme inhibitor URB597 decreased restraint-evoked tachycardia. Inhibition of the hydrolysis of 2-arachidonoylglycerol (2-AG) in the BNST by local microinjection of the MAGL enzyme inhibitor JZL184 also decreased the HR response. These effects of URB597 and JZL184 were abolished by BNST pretreatment with AM251. CONCLUSIONS AND IMPLICATIONSThese findings indicate an involvement of BNST endocannabinoid neurotransmission, acting via CB 1 receptors, in cardiovascular adjustments during emotional stress, which may be mediated by the local release of either AEA or 2-AG.Abbreviations 2-AG, 2-arachidonoylglycerol; AEA, anandamide or arachidonoylethanolamide; BNST, bed nucleus of the stria terminalis; CBD, cannabidiol; CRF, corticotropin-releasing factor; DBP, diastolic blood pressure; FAAH, fatty acid amide hydrolase; HR, heart rate; MAGL, monoacylglycerol lipase; MBP, mean blood pressure; MPFC, medial prefrontal cortex; NTS, nucleus of the solitary tract; PAG, periaqueductal gray; PVN, hypothalamic paraventricular nucleus; RVLM, rostral ventrolateral medulla; TRPV1, transient receptor potential vanilloid 1; Δ 9 -THC, Δ 9 -tetrahydrocannabinol

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Section: Discussionmentioning

confidence: 99%

Involvement of endocannabinoid neurotransmission in the bed nucleus of stria terminalis in cardiovascular responses to acute restraint stress in rats

Gomes‐de‐Souza

Oliveira

Benini

et al. 2016

British J Pharmacology

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“…In the Vicious Cycle of Stress, the right arc of the cycle represents the influence of stress on disease. Countless studies have experimentally demonstrated the negative impact stress has on disease progression, from cancer to cardiovascular disease, neurodegenerative disease and symptoms of aging (for review, see: Bjorntorp, 1997 ; Wahrborg, 1998 ; Girod and Brotman, 2004 ; Reiche et al, 2004 ; DiMicco et al, 2006 ; Pasquali et al, 2006 ; Goosens and Sapolsky, 2007 ; El Husseini and Laskowitz, 2014 ; Gupta and Morley, 2014 ; Prenderville et al, 2015 ; Herbert and Lucassen, 2016 ; Martocchia et al, 2016 ; Shin et al, 2016 ; Bortolato et al, 2017 ; Crestani, 2017 ). However, there are far fewer studies that address the left arc of the cycle.…”

Section: The Relationship Between Stress and Neurodegenerative Diseasmentioning

confidence: 99%

The relationship between stress and Alzheimer's disease

Justice

2018

Neurobiology of Stress

186

119

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Stress is critically involved in the development and progression of disease. From the stress of undergoing treatments to facing your own mortality, the physiological processes that stress drives have a serious detrimental effect on the ability to heal, cope and maintain a positive quality of life. This is becoming increasingly clear in the case of neurodegenerative diseases. Neurodegenerative diseases involve the devastating loss of cognitive and motor function which is stressful in itself, but can also disrupt neural circuits that mediate stress responses. Disrupting these circuits produces aberrant emotional and aggressive behavior that causes long-term care to be especially difficult. In addition, added stress drives progression of the disease and can exacerbate symptoms. In this review, I describe how neural and endocrine pathways activated by stress interact with ongoing neurodegenerative disease from both a clinical and experimental perspective.

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“…However, independently of the chronic stress paradigm, a similar small hypertensive effect (~10 mm Hg) was observed following long-term stress exposure in studies wherein baseline mean arterial pressure in control groups ranged from 95 to 120 mmHg (Grippo et al, 2008 ; Daubert et al, 2012 ; Duarte et al, 2015a ; Cruz et al, 2016 ) (Table 1 ). It has also been documented that cardiovascular dysfunctions induced by chronic stressors may be related to animals age (Crestani, 2016 ); hence, an influence of age (e.g., young vs. adult) was considered in this review (Table 1 ). However, the influence of age seems to be related to the type of chronic stressor.…”

Section: Cardiovascular Responses To Stress: Influence Of Chronicitymentioning

confidence: 99%

Emotional Stress and Cardiovascular Complications in Animal Models: A Review of the Influence of Stress Type

Crestani

2016

Front. Physiol.

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Emotional stress has been recognized as a modifiable risk factor for cardiovascular diseases. The impact of stress on physiological and psychological processes is determined by characteristics of the stress stimulus. For example, distinct responses are induced by acute vs. chronic aversive stimuli. Additionally, the magnitude of stress responses has been reported to be inversely related to the degree of predictability of the aversive stimulus. Therefore, the purpose of the present review was to discuss experimental research in animal models describing the influence of stressor stimulus characteristics, such as chronicity and predictability, in cardiovascular dysfunctions induced by emotional stress. Regarding chronicity, the importance of cardiovascular and autonomic adjustments during acute stress sessions and cardiovascular consequences of frequent stress response activation during repeated exposure to aversive threats (i.e., chronic stress) is discussed. Evidence of the cardiovascular and autonomic changes induced by chronic stressors involving daily exposure to the same stressor (predictable) vs. different stressors (unpredictable) is reviewed and discussed in terms of the impact of predictability in cardiovascular dysfunctions induced by stress.

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Adolescent vulnerability to cardiovascular consequences of chronic emotional stress: Review and perspectives for future research

Cited by 17 publications

References 113 publications

Involvement of endocannabinoid neurotransmission in the bed nucleus of stria terminalis in cardiovascular responses to acute restraint stress in rats

Involvement of endocannabinoid neurotransmission in the bed nucleus of stria terminalis in cardiovascular responses to acute restraint stress in rats

The relationship between stress and Alzheimer's disease

Emotional Stress and Cardiovascular Complications in Animal Models: A Review of the Influence of Stress Type

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