scholarly journals κ-Opioid receptors in the infralimbic cortex modulate the cardiovascular responses to acute stress

2015 ◽  
Vol 100 (4) ◽  
pp. 377-387 ◽  
Author(s):  
Aline Fassini ◽  
América A. Scopinho ◽  
Leonardo B. M. Resstel ◽  
Fernando M. A. Corrêa
2021 ◽  
Author(s):  
Siobhán M Griffin ◽  
Siobhán Howard

Instructed use of reappraisal to regulate stress in the laboratory is typically associated with a more adaptive cardiovascular response to stress, indexed by either: (i) lower cardiovascular reactivity (CVR; e.g., lower blood pressure); or (ii) a challenge-oriented response profile (i.e., greater cardiac output paired with lower total peripheral resistance). In contrast, instructed use of suppression is associated with exaggerated CVR (e.g., greater heart rate, blood pressure). Despite this, few studies have examined if the habitual use of these strategies are related to cardiovascular responding during stress. The current study examined the relationship between cardiovascular responses to acute stress and individual differences in emotion regulation style: trait reappraisal, suppression, and emotion regulation difficulties. Forty-eight participants (25 women, 23 men) completed a standardised laboratory stress paradigm incorporating a 20-minute acclimatization period, a 10-minute baseline, and two 5-minute speech tasks separated by a 10-minute inter-task rest period. The emotional valence of the speech task was examined as a potential moderating factor; participants spoke about a block of negative-emotion words and a block of neutral-emotion words. Cardiovascular parameters were measured using the Finometer Pro. Greater habitual use of suppression was associated with exaggerated blood pressure responding to both tasks. However, only in response to the negative-emotion task was greater use of reappraisal associated with a challenge-oriented cardiovascular response. The findings suggest that individual differences in emotion regulation translate to differing patterns of CVR to stress, but the emotional valence of the stressor may play a role.


2016 ◽  
Vol 53 (5) ◽  
pp. 739-748 ◽  
Author(s):  
Andrew J. Wawrzyniak ◽  
Mark Hamer ◽  
Andrew Steptoe ◽  
Romano Endrighi

2009 ◽  
Vol 21 (1) ◽  
pp. 207-225 ◽  
Author(s):  
Brooks B. Gump ◽  
Jacki Reihman ◽  
Paul Stewart ◽  
Ed Lonky ◽  
Tom Darvill ◽  
...  

AbstractMaternal depression has a number of adverse effects on children. In the present study, maternal depressive symptoms were assessed (using the Center for Epidemiological Studies Depression Scale) when their child was 3 months, 6 months, 1 year, 2 years, 4.25 years, 6 years, 7 years, 8 years, and 10 years of age. At 9.5 years of age, children's (94 females, 82 males) depressive symptoms as well as cardiovascular and cortisol levels during baseline and two psychologically stressful tasks were measured. Using multilevel modeling, maternal depressive symptom trajectories were considered in relation to their child's adrenocortical and cardiovascular responses to acute stress. Our goal was to determine maternal depressive symptom trajectories for children with elevated cardiovascular and cortisol reactivity to acute stress and elevated depressive symptoms. In general, those mothers with chronically elevated depressive symptoms over their child's life span had children with lower initial cortisol, higher cardiac output and stroke volume in response to acute stress, lower vascular resistance during acute stress tasks, and significantly more depressive symptoms at 9.5 years of age. These results are discussed in the context of established associations among hypothalamic–pituitary–adrenal axis dysregulation, depression, and cardiovascular disease.


Stress ◽  
2009 ◽  
pp. 1-1 ◽  
Author(s):  
Agnieszka Wsoł ◽  
Agnieszka Cudnoch-JĘdrzejewska ◽  
Ewa Szczepanska-Sadowska ◽  
Stanisław Kowalewski ◽  
Jakub Dobruch

Hypertension ◽  
1996 ◽  
Vol 27 (4) ◽  
pp. 962-967 ◽  
Author(s):  
Paul J. Mills ◽  
Richard A. Nelesen ◽  
Michael G. Ziegler ◽  
Barbara L. Parry ◽  
Charles C. Berry ◽  
...  

2015 ◽  
Vol 308 (6) ◽  
pp. H612-H622 ◽  
Author(s):  
Benedek Erdos ◽  
Iara Backes ◽  
Michael L. McCowan ◽  
Linda F. Hayward ◽  
Deborah A. Scheuer

Brain-derived neurotrophic factor (BDNF) expression increases in the paraventricular nucleus of the hypothalamus (PVN) in response to hypertensive stimuli including stress and hyperosmolarity. However, it is unclear whether BDNF in the PVN contributes to increases in blood pressure (BP). We tested the hypothesis that increased BDNF levels within the PVN would elevate baseline BP and heart rate (HR) and cardiovascular stress responses by altering central angiotensin signaling. BP was recorded using radiotelemetry in male Sprague-Dawley rats after bilateral PVN injections of adeno-associated viral vectors expressing green fluorescent protein (GFP) or myc epitope-tagged BDNF fusion protein. Cardiovascular responses to acute stress were evaluated 3 to 4 wk after injections. Additional GFP and BDNF-treated animals were equipped with osmotic pumps for intracerebroventricular infusion of saline or the angiotensin type-1 receptor (AT1R) inhibitor losartan (15 μg·0.5 μl−1·h−1). BDNF treatment significantly increased baseline BP (121 ± 3 mmHg vs. 99 ± 2 mmHg in GFP), HR (394 ± 9 beats/min vs. 314 ± 4 beats/min in GFP), and sympathetic tone indicated by HR- and BP-variability analysis and adrenomedullary tyrosine hydroxylase protein expression. In contrast, body weight and BP elevations to acute stressors decreased. BDNF upregulated AT1R mRNA by ∼80% and downregulated Mas receptor mRNA by ∼50% in the PVN, and losartan infusion partially inhibited weight loss and increases in BP and HR in BDNF-treated animals without any effect in GFP rats. Our results demonstrate that BDNF overexpression in the PVN results in sympathoexcitation, BP and HR elevations, and weight loss that are mediated, at least in part, by modulating angiotensin signaling in the PVN.


2016 ◽  
Vol 3 ◽  
pp. 23-33 ◽  
Author(s):  
Kelly M. Moench ◽  
Mouna Maroun ◽  
Alexandra Kavushansky ◽  
Cara Wellman

1994 ◽  
Vol 56 (4) ◽  
pp. 709-713 ◽  
Author(s):  
Brian J. Sanders ◽  
Carrie Wirtz-Nole ◽  
S.Michelle DeFord ◽  
Brian F. Erling

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