Stress and Addiction
Hanna Pickard, Serge H. Ahmed in The Routledge Handbook of Philosophy and Science of Addiction, 2019
The above brain stress responses coordinate our well-known “fight” or “flight” response, which produce stress sensations such as the heart beating faster, breathing faster, mobilizing energy stores and inflammatory responses, via the hypothalamic-pituitary-adrenal (HPA) axis that signals to produce cortisol, and the autonomic nervous system that mobilizes heart rate and blood pressure arousal, and also immune responses. These physiological arousal pathways signal the body and the brain to coordinate and modulate the behavioral, cognitive and learning aspects of the stress response. The HPA axis is stimulated by the corticotropin releasing factor (CRF), released from the paraventricular nucleus (PVN) of the hypothalamus, to stimulate the adrenocorticotrophin hormone from the anterior pituitary that initiates the secretion of cortisol/corticosterone from the adrenal glands. The autonomic nervous system includes the sympathetic nervous system that mobilizes the cardiovascular and immune arousal responses, and the parasympathetic nervous system that is involved in regulating the sympathetic arousal by providing the ‘brakes’ to the sympathetic arousal and in regaining homeostasis via the sympathoadrenal medulary (SAM) pathways. Recent evidence also indicates that the sympathetic pathways provide further modulation of the adrenal glands for release of cortisol as well as release of norepinephrine and epinephrine. These are the core stress pathways involved in stress arousal and mobilization of the body and brain to respond to stress and in regulation of stress so as to regain homeostasis.
Adaptation to Stress and its Cardioprotective Effect in Stress, Ischemic, and Reperfusion Damage
Felix Z. Meerson, Alexander V. Galkin in Adaptive Protection of The Heart: Protecting Against Stress and Ischemic Damage, 2019
It further turned out that the lack of blood corticosteroid elevation in response to heavy stress in adapted animals, i.e., “fading” of the adrenocortical link of the stress reaction, also does not result from exhaustion of the functional resources of the adrenal cortex. On the opposite, injected ACTH causes a much greater elevation of blood corticosterone in stress-adapted than in nonadapted animals.18 This is important evidence that adaptation involves (1) increased power of the adrenocortical link of the stress-effecting sympathoadrenal system and (2) altered organismic reaction to stress at the central level, i.e., at the level of releasing factors and ACTH. It is at this level that some mechanisms are actuated by adaptation and, despite the stress, hinder the output of releasing factors and tropic hormones, and prevent increased secretion of stress hormones and mediators (in this case corticosterone).
The Role of the Renal Nerves in the Pathogenesis of Hypertension*
Irving H. Zucker, Joseph P. Gilmore in Reflex Control of the Circulation, 2020
To test the hypothesis that the renal afferent nerves modulate sympathetic nervous system activity, and thereby contribute to the maintenance of hypertension in the 1K,1C model, the effects of environmental stress on plasma norepinephrine and epinephrine levels were compared in hypertensive sham-operated, renal-denervated, and control rats (Katholi et al., 1982a). Stress was produced in conscious resting unrestrained rats by administering two brief electrical stimulations to the hindlimb. Resting plasma norepinephrine was significantly higher (p < 0.01) in hypertensive sham-operated compared to renal-denervated or control rats, but there was no difference in resting plasma epinephrine among the groups. In response to stress, there were significantly greater absolute increases in plasma norepinephrine and epinephrine in hypertensive sham-operated animals than in renal-denervated and control groups, suggesting that the 1K,1C hypertensive rat exhibits an enhanced sympathoadrenal response to stress. The response to stress in renal-denervated rats was the same as that in the normotensive control group. These data support the concept that the renal-afferent nerves modulate sympathetic nervous system activity in the 1K,1C hypertensive rat.
Stress and social isolation, and its relationship to cardiovascular risk in young adults with intellectual disability
Published in Disability and Rehabilitation, 2023
Clara C. Zwack, Rachael McDonald, Ainura Tursunalieva, Shradha Vasan, Gavin W. Lambert, Elisabeth A. Lambert
Broadly speaking there are two kinds of stress, each with different physiological and psychological effects. Acute stress is when stress is experienced for a short period of time- for example an argument with a loved one, being stuck in a traffic jam or receiving criticism from an employer. Chronic stress results from repeated exposure to stressors such as a relationship break-down, job strain [15]1, loneliness and social isolation. Long-term chronic exposure to stress has been related to a 40–60% excess risk of incident coronary heart disease (CHD) [16]. Stress produces many physiological changes, some of which may contribute to the development of CVD. Stress reactivity to everyday events activates both the sympathetic nervous system (SNS), sympathoadrenal (SA) axis and the hypothalamic-pituitary-adrenocortical (HPA) axis. This in turn leads to mobilisation of stored energy, increased heart rate and peripheral vasoconstriction, and multiple other physiological effects [17].
The neurobiology of childhood trauma—aldosterone and blood pressure changes in a community sample
Published in The World Journal of Biological Psychiatry, 2022
Jan Terock, Anke Hannemann, Johanna Klinger-König, Deborah Janowitz, Hans J. Grabe, Harald Murck
The renin-angiotensin-aldosterone-system (RAAS) is the key hormonal system for blood pressure regulation and sodium balance and specifically mediates the blood pressure response to stress exposure (Aguilera et al. 1995). It closely interacts with the sympathoadrenal-medullary (SAM-)system and the hypothalamic-pituitary-adrenal (HPA-)axis in the body’s stress response to acute and chronic stressors (Groeschel and Braam 2011). Acute stress leads to the activation of the SAM-system, which stimulates the excretion of renin, which is followed by increases in angiotensin II (ANG II) and finally aldosterone. Aldosterone is an important agent for the reabsorption of sodium and water and thereby for the blood pressure regulation and plays a prominent role in the initiation of the stress response and stress-induced depressive behaviour (Hlavacova and Jezova 2008; Hlavacova et al. 2012; Franklin et al. 2015; Terock et al. 2017).
Childhood-onset craniopharyngioma: latest insights into pathology, diagnostics, treatment, and follow-up
Published in Expert Review of Neurotherapeutics, 2018
Agnieszka Bogusz, Hermann L. Müller
Hypothalamic obesity in childhood-onset CP patients is mainly unresponsive to conventional treatment options such as lifestyle modifications (diet and exercise) for regulating body composition due to imbalances in central sympathetic output, energy expenditure, and dysregulation of appetite. Pharmacological treatment with dextroamphetamine has been suggested in these conditions based on observed reductions in sympathoadrenal activation and epinephrine production. A study on dextroamphetamine therapy initiated 10 months after surgery for a 24-month treatment period reported on significantly decreased weight gain and stabilization body mass index [96]. Furthermore, a significant increase of spontaneous physical activity was observed. Improvements of daytime sleepiness have been reported after even shorter periods of dextroamphetamine medication [97]. Elfers and Roth reported on beneficial effects of the central stimulating agent methylphenidate on the stabilization of weight development and prevention of severe obesity in childhood-onset CP patients [98].
Related Knowledge Centers
- Adrenal Medulla
- Adrenaline
- Postganglionic Nerve Fibers
- Sympathetic Nervous System
- Norepinephrine
- Homeostasis
- Acetylcholine
- Hypoglycemia
- Preganglionic Nerve Fibers
- Fight-Or-Flight Response