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Endocrine Functions of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Whereas the above studies demonstrated that peripheral DA responds strongly to stressful stimuli, the specific targets of circulating DA and the physiological parameters that it alters are presently unknown. The other two catecholamines regulate a wide variety of physiological effects, from increases in heart rate and blood pressure to energy release and blood flow to the skeletal muscle, all as part of the “fight or flight” response. However, the effects of DA on any of these parameters are mild at best, and in some vascular beds, DA reduces, rather than elevates, blood pressure. One potential target for the stress-elevated peripheral DA is the activation of the HPA axis, by acting on the pituitary and/or the adrenals. In the human pituitary, D2Rs are expressed at moderate levels in ACTH-producing corticotrophs, while D1R-like and D2R-like receptors are expressed in all three zones of the normal human adrenal cortex [31]. Future studies that address these issues should be undertaken.
Summation of Basic Endocrine Data
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Stress activates the sympathetic nervous system to release catecholamines from the nerve endings. The release is increased in darkness and the pineal gland becomes involved. The gland is stimulated by adrenal medullary or neural hormones in that their secretions bind to p-adrenergic receptors. This activates adenylate cyclase and leads to the production of cAMP, then protein kinases, and finally the involvement of enzymes essential to the synthesis of melatonin. Most of the melatonin secretion occurs at night as part of a circadian cycle.
The Influence of Pituitary-Adrenal Axis on the Immune System
Published in Istvan Berczi, Pituitary Function and Immunity, 2019
Epinephrine (or adrenaline), norepinephrine (or noradrenaline), and dopamine are commonly referred to as catecholamines because of their structural relationship and common biosynthetic pathways. Catecholamines are synthesized in the brain, in sympathetic nerve endings, and in some cells of neural crest origin: the adrenal medulla and the organ of Zuckerkandl. Catecholamines have profound effects on smooth muscle, adipose tissue, myocardium, liver, brain, formed elements of the blood, a number of hormone producing organs, and the myometrium. Although the thymus and spleen both have innervation and the lymphoid cells residing in these organs may well be exposed to catecholamines secreted by nerve endings, the cells in the blood are exposed only to circulating catecholamines and are not influenced by the neuronally-derived catecholamines released in other tissues.
Subarachnoidal hemorrhage related cardiomyopathy: an overview of Tako-Tsubo cardiomyopathy and related cardiac syndromes
Published in Expert Review of Cardiovascular Therapy, 2022
Susan Deenen, Dharmanand Ramnarain, Sjaak Pouwels
Heart failure including TTS is a well-recognized complication of neurologic diseases. In normal physiology, the parasympathetic and sympathetic nervous systems have an important role in the regulation of cardiac function [5,15]. The nervus vagus mediates the parasympathetic stimulation of the heart and leads to decreased heart rate, atrioventricular (AV) conduction, and ventricular excitability. Sympathetic stimulation leads to increased heart rate, AV conduction, and ventricular excitability and contractility. Also, the higher cerebral structures such as the frontal cortex, insula, amygdala, cingulate, hypothalamus, and periaqueductal gray matter influence cardiac function [5]. Furthermore, the hypothalamic–pituitary–adrenal axis (neuroendocrine system) influences the cardiac system by creating a stress response and thereby releasing cortisol and catecholamines. Catecholamines influence adrenergic receptors (ARs), leading to increased heart rate, contraction, and changes in blood pressure [5]. How these pathways can be disrupted by neurological injury and thereby cause cardiac dysfunction is a complex process, and many theories are mentioned. However, most recent studies describe an important role for catecholamines [5,9,12,13]. This theory is generally believed to explain the pathophysiology of cardiac dysfunction in SAH patients. SAH can cause mild-to-severe cardiac dysfunction in the form of ECG changes, arrhythmias, LV dysfunction, and release of cardiac biomarkers. In SAH patients with elevated catecholamine levels, it is also described that cardiac enzymes are elevated [1,2,5,12,13].
Racial discrimination and disability among Asian and Latinx populations in the United States
Published in Disability and Rehabilitation, 2022
Kyle Waldman, Andrew Stickley, Beverly Araujo Dawson, Hans Oh
Various biological mechanisms may provide one of many possible explanations for the association between racial discrimination and disability among the respondents who report both limitations in functioning and physical and/or mental health diagnoses [77]. Discrimination is a stressor [5], and stressors activate the parasympathetic and sympathetic nervous system in an attempt to stimulate the body’s defenses. The “psychobiological reactivity” perspective posits that the immune, endocrine, and cardiovascular responses to psychosocial stress are interconnected [78,79]. Cumulatively, repeated exposure to stress may interrupt bodily homeostasis via activation of those systems and contribute to the accumulation of excess allostatic load [80], which in turn, causes “wear and tear” on the body, and predisposes humans to illness [81], including cardiovascular disease, stroke, abdominal obesity, and suppression of immune functions [82]. Additionally, discrimination may precipitate pathophysiologic alterations in the body by recurrently activating the hypothalamic-pituitary-adrenal (HPA) axis, resulting in a release of excess cortisol and catecholamines [83]. Cortisol has been linked to hypertension, central adiposity [84], and cognitive impairment [85]. Catecholamines have been associated with a greater risk of hypertension, stroke, and myocardial infarction [85]. Repeated activation of the stress response systems can also result in neuroinflammation in different areas of the brain, increasing the likelihood of developing mental illness [86] and cognitive or functional impairments [87,88].
Tissue and interspecies comparison of catechol-O-methyltransferase mediated catalysis of 6-O-methylation of esculetin to scopoletin and its inhibition by entacapone and tolcapone
Published in Xenobiotica, 2021
Aaro Jalkanen, Veera Lassheikki, Tommi Torsti, Elham Gharib, Marko Lehtonen, Risto O. Juvonen
The catechol compounds have both beneficial and adverse health effects in humans (Cavalieri et al.2006; Yang et al.2014; Sanders-Bush and Hazelwood 2015). Catecholamines are important neurotransmitters and regulators in the central and peripheral nervous system (Sanders-Bush and Hazelwood 2015). They are also key intermediate compounds when the melanin pigment is synthesised to protect skin against UV-light (Slominski et al.2004) or in substantia nigra (Zucca et al.2014). Other catechol compounds, such as flavonoids, are well-recognised antioxidants (Alfa and Arroo 2019). On the other hand, the catechol structure can be oxidised by CYP or peroxidase enzymes to an electrophilic quinone or semiquinone (Cavalieri et al.2004, 2006). These metabolites can react with macromolecules such as proteins or nucleic acids causing toxicity. Under suitable conditions, catechol, semiquinone, and quinone can form a self-serving catalytic cycle leading to an excessive production of reactive oxygen species evoking oxidative stress. For this reason, catechol compounds are potentially toxic and may cause adverse health effects such as cell death, mutations, and cancer. The methylation of the catechol structure to a hydroxyl-methoxy benzene derivative prevents the formation of the quinone or semiquinone and thus reduces the reactivity of catechol compounds (Zhu 2004; Yager 2012).