Cynical hostility relates to a lack of habituation of the cardiovascular response to repeated acute stress

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.

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AEROBIC TRAINING ALTERS THE CARDIOVASCULAR RESPONSE TO ACUTE STRESS IN AFRICAN AMERICAN WOMEN 996

Medicine & Science in Sports & Exercise ◽

10.1097/00005768-199705001-00995 ◽

1997 ◽

Vol 29 (Supplement) ◽

pp. 174

Author(s):

V. Bond ◽

M. Roltsch ◽

M. Caprarola ◽

T. Mendez ◽

P. Vaccaro ◽

...

Keyword(s):

African American ◽

African American Women ◽

Aerobic Training ◽

Acute Stress ◽

Cardiovascular Response ◽

American Women

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Acute stress increases venomotor tone in conscious rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.271.4.h1375 ◽

1996 ◽

Vol 271 (4) ◽

pp. H1375-H1383 ◽

Cited By ~ 2

Author(s):

D. S. Martin ◽

C. Appelt ◽

M. C. Rodrigo ◽

M. C. Egland

Keyword(s):

Psychological Stress ◽

Acute Stress ◽

Cardiovascular Response ◽

Pressor Response ◽

Venous Pressure ◽

Receptor Subtype ◽

Indwelling Catheters ◽

Conscious Rats ◽

Air Jet ◽

Acute Psychological Stress

This study tested the hypothesis that acute psychological stress causes venoconstriction. Male Sprague-Dawley rats were instrumented with indwelling catheters in a femoral artery and vein and a balloon-tipped catheter in the right atrium. Mean arterial pressure (MAP), venous pressure, heart rate (HR), and mean circulatory filling pressure (MCFP) were monitored in conscious rats. Air-jet stress was performed before and after treatment with saline, chlorisondamine, phentolamine, or prazosin. Air-jet stress caused MAP, HR, and MCFP to increase by 10 +/- 1 mmHg, 31 +/- 4 beats/min, and 0.95 +/- 0.09 mmHg, respectively. Treatment with either chlorisondamine or phentolamine was equally effective in abolishing the stress-induced increases in MAP, HR, and MCFP. Prazosin treatment abolished the pressor response to air-jet stress but did not significantly affect the HR and MCFP responses. In contrast, pretreatment with the alpha 2-receptor antagonist rauwolscine hydrochloride abolished both the MAP and MCFP responses to air-jet stress but did not affect the HR response. These findings indicate that venoconstriction is an important component of the cardiovascular response to acute psychological stress. Stress-induced venoconstriction appears to be mediated primarily via the alpha 2-receptor subtype.

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Effects of perinatal oxycodone exposure on the cardiovascular response to acute stress in male rats at weaning and in young adulthood

Frontiers in Physiology ◽

10.3389/fphys.2013.00085 ◽

2013 ◽

Vol 4 ◽

Cited By ~ 6

Author(s):

Thitinart Sithisarn ◽

Henrietta S. Bada ◽

Richard J. Charnigo ◽

Sandra J. Legan ◽

David C. Randall

Keyword(s):

Young Adulthood ◽

Acute Stress ◽

Cardiovascular Response ◽

Male Rats

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Central tachykinins: mediators of defence reaction and stress reactions

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y95-122 ◽

1995 ◽

Vol 73 (7) ◽

pp. 885-891 ◽

Cited By ~ 77

Author(s):

Juraj Culman ◽

Thomas Unger

Keyword(s):

Substance P ◽

Acute Stress ◽

Cardiovascular Response ◽

Neurokinin A ◽

Endocrine Regulation ◽

Stress Reactions ◽

Defence Reaction ◽

Renal Vasoconstriction ◽

Sympathoadrenal Activity ◽

The Brain

The tachykinins substance P, neurokinin A, and neurokinin B are natural agonists for NK1, NK2, and NK3 receptors, respectively. Evidence from biochemical, neurophysiological, pharmacological, and molecular biology studies indicates that the tachykinin-containing pathways within the brain contribute to central cardiovascular and endocrine regulation and to the control of motor activity. The hypothalamus, which represents a site for the integration of central neuroendocrine and autonomic processes, is rich in tachykinin nerve endings and tachykinin receptors. Stimulation of periventricular or hypothalamic NK1 receptors in conscious rats induces an integrated cardiovascular, behavioural, and endocrine response. The cardiovascular response is associated with increased sympathoadrenal activity and comprises an increase in blood pressure and heart rate, mesenteric and renal vasoconstriction, and hind-limb vasodilatation. The behavioural response consists of increased locomotion and grooming behaviour. This response pattern is consistent with an integrated stress response to nociceptive stimuli and pain in rodents. Several studies have demonstrated rapid changes in substance P levels and its receptors in distinct brain areas following acute stress. These data indicate that substance P and other tachykinins, in addition to serving as nociceptive and pain transmitters in the spinal cord, may act in the brain as neurotransmitters–neuromodulators within the neuronal circuits mediating central stress responses.Key words: tachykinins, substance P, central nervous system, defence reaction, stress.

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Hemodynamic response pattern predicts susceptibility to stress-induced elevation in arterial pressure in the rat

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2001.281.1.r31 ◽

2001 ◽

Vol 281 (1) ◽

pp. R31-R37 ◽

Cited By ~ 21

Author(s):

Jay R. Muller ◽

Khoi M. Le ◽

William R. Haines ◽

Qi Gan ◽

Mark M. Knuepfer

Keyword(s):

Cardiac Output ◽

Conditioned Stimulus ◽

Arterial Pressure ◽

Vascular Resistance ◽

Acute Stress ◽

Cardiovascular Response ◽

Cardiovascular Responses ◽

Response Patterns ◽

Air Jet ◽

Poststress Period

Cocaine or air jet stress evokes pressor responses due to either a large increase in systemic vascular resistance (vascular responders) or small increases in both cardiac output and vascular resistance (mixed responders) in conscious rats. Repeated cocaine administration results in elevated arterial pressure in vascular responders but not in mixed responders. The present study examined the hypothesis that the pattern of cardiovascular responses to an unconditioned stimulus (UCS; air jet) is related to responses to a conditioned stimulus (CS; tone followed by brief foot shock) in individual rats. Our data demonstrate that presentation of the UCS produced variable cardiac output responses that correlated with responses to the CS ( n = 60). We also determined whether individual cardiovascular response patterns to acute stress correlated with predisposition to a sustained stress-induced elevation in arterial pressure. Rats were exposed to three different stressors presented one per day successively for 4 wk and during a poststress period of 3 wk while arterial pressure was recorded periodically. Mean arterial pressure was elevated in all rats during chronic stress but, during the poststress period, remained at significantly higher levels in vascular responders but not mixed responders. Therefore, we conclude that acute behavioral stress to a conditioned stimulus elicits variable hemodynamic responses that predict the predisposition to a sustained stress-induced elevation in arterial pressure.

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Activation of angiotensin-converting enzyme 2/angiotensin-(1–7)/Mas axis attenuates the cardiac reactivity to acute emotional stress

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00433.2013 ◽

2013 ◽

Vol 305 (7) ◽

pp. H1057-H1067 ◽

Cited By ~ 33

Author(s):

Augusto Martins Lima ◽

Carlos Henrique Xavier ◽

Anderson José Ferreira ◽

Mohan K. Raizada ◽

Gerd Wallukat ◽

...

Keyword(s):

Angiotensin Converting Enzyme ◽

Intravenous Injection ◽

Emotional Stress ◽

Acute Stress ◽

Cardiovascular Response ◽

Cardiovascular Responses ◽

Converting Enzyme ◽

Angiotensin Converting Enzyme 2 ◽

Air Jet ◽

Acute Emotional Stress

Recent data indicate the brain angiotensin-converting enzyme/ANG II/AT1 receptor axis enhances emotional stress responses. In this study, we investigated whether its counterregulatory axis, the angiotensin-converting enzyme 2 (ACE2)/ANG-(1–7)/Mas axis, attenuate the cardiovascular responses to acute emotional stress. In conscious male Wistar rats, the tachycardia induced by acute stress (air jet 10 l/min) was attenuated by intravenous injection of ANG-(1–7) [Δ heart rate (HR): saline 136 ± 22 vs. ANG-(1–7) 61 ± 25 beats/min; P < 0.05]. Peripheral injection of the ACE2 activator compound, XNT, abolished the tachycardia induced by acute stress. We found a similar effect after intracerebroventricular injections of either ANG-(1–7) or XNT. Under urethane anesthesia, the tachycardia evoked by the beta-adrenergic agonist was markedly reduced by ANG-(1–7) [ΔHR: saline 100 ± 16 vs. ANG-(1–7) 18 ± 15 beats/min; P < 0.05]. The increase in renal sympathetic nerve activity (RSNA) evoked by isoproterenol was also abolished after the treatment with ANG-(1–7) [ΔRSNA: saline 39% vs. ANG-(1–7) −23%; P < 0.05]. The tachycardia evoked by disinhibition of dorsomedial hypothalamus neurons, a key nucleus for the cardiovascular response to emotional stress, was reduced by ∼45% after intravenous injection of ANG-(1–7). In cardiomyocyte, the incubation with ANG-(1–7) (1 μM) markedly attenuated the increases in beating rate induced by isoproterenol. Our data show that activation of the ACE2/ANG-(1–7)/Mas axis attenuates stress-induced tachycardia. This effect might be either via the central nervous system reducing anxiety level and/or interfering with the positive chronotropy mediated by activation of cardiac β adrenergic receptors. Therefore, ANG-(1–7) might contribute to reduce the sympathetic load to the heart during situations of emotional stress, reducing the cardiovascular risk.

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