A Biopsychosocial Approach to Anxiety
Stephen M. Stahl, Bret A. Moore in Anxiety Disorders: A Guide for Integrating Psychopharmacology and Psychotherapy, 2013
Noradrenaline or norepinephrine (NE) is a catecholamine that functions as a hormone and a neurotransmitter. As a neurotransmitter, NE is released in response to stressful stimuli and affects a variety of body systems throughout the central nervous system and cardiovascular system. Specifically, it directly causes increased heart rate, along with increasing energy utilization, during the “fight or flight” response (Guyton & Hall, 2006). In the brain, NE is synthesized in the adrenal medulla, post-ganglionic neurons of the sympathetic nervous system, and the locus coeruleus, a region of the brain stem and the origin of norepinephrine pathways in the central nervous system. Pathways from the locus coeruleus act on adrenergic receptors in regions of the limbic system and cerebral cortex (O'Donnell, Hegadoren, & Coupland, 2004). In response to threat, the locus coeruleus is activated by the amygdala and hypothalamus. NE is then released and stimulates several limbic and cortical regions to mediate an appropriate adaptive response to threatening stimuli. Clinical studies demonstrate that an exaggerated release of NE in response to threat results in anxiety symptoms such as panic attacks, hyperarousal, exaggerated startle, and insomnia (reviewed by Southwick et al., 1999).
Prejunctional Dopamine Receptor Stimulants
M.D. Francesco Amenta in Peripheral Dopamine Pathophysiology, 2019
Numerous studies in normotensive subjects have confirmed the thesis that stimulation of prejunctional DA receptors has a significant effect on noradrenaline release from sympathetic neurones in man. Bromocriptine reduces plasma noradrenaline levels by up to 60% in the supine and standing position,93-104 and also depresses the increases that occur in response to exercise on the bicycle ergometer,93 isometric hand-grip exercise,97,99 sodium depletion,98 and graded lower body negative pressure.105 Pretreatment with metoclopramide or domperidone prevents bromocriptine-induced reductions in noradrenaline levels in both supine and upright positions, confirming the peripheral dopaminomimetic nature of the effect.101 Effects on noradrenaline levels are associated with decreases in blood pressure and peripheral vascular resistance and an increase in venous distensibility, with little change or small decreases in heart rate.94,100 These findings suggest that a drug acting on peripheral DA2 receptors might be of use clinically in certain cardiovascular disorders.
Drugs Affecting Storage and Release from Sympathetic Neurones
Kenneth J. Broadley in Autonomic Pharmacology, 2017
Side-effects of α-methyldopa arise most commonly from its central site of action and include sedation and drowsiness. This is particularly troublesome in individuals requiring a high level of mental concentration in their work and may lead to absentmindedness and mental confusion. Other rare signs of disturbed CNS metabolism of noradrenaline include Parkinsonism, nightmares, headache and depression. Mild block of peripheral sympathetic output may also lead to uncommon side-effects such as dry mouth, nasal stuffiness, ejaculation failure, bradycardia and postural hypotension. A rare but serious side-effect is haemolytic anaemia due to the development of an autoimmune response. The antibodies are directed against the patient’s erythrocytes which are destroyed. Twenty percent of patients receiving αmethyldopa for a year produced a positive Coomb’s test, which detects the antibodies, but only 1–5% of these patients develop haemolytic anaemia. Leucopaenia, thrombocytopaenia, hepatitis and fever are also rare side-effects. Gynaecomastia (breast enlargement) and lactation occur due to interference with dopaminergic suppression of prolactin secretion. α-Methyldopa is contraindicated in liver disease, depression and phaeochromocytoma, the latter being exacerbated because of further increases in plasma catecholamines. Because of these adverse effects, α-methyldopa is no longer a drug of first choice in the routine management of hypertension.
Renal and Hepatic Disease: Cnidoscolus aconitifolius as Diet Therapy Proposal for Prevention and Treatment
Published in Journal of the American College of Nutrition, 2021
Maria Lilibeth Manzanilla Valdez, Maira Rubi Segura Campos
The treatment with vasoconstrictors and albumin is one of the first options to choose. The goal of treatment is to produce vasoconstriction in the splenic vascular bed and reduce hypovolemia.Alpha adrenergic agonists: norepinephrine, midrodine. Norepinephrine is a catecholamine that acts on adrenergic receptors. Midodrine acts as a selective agonist of peripheral alpha-1 receptors, generating vasoconstriction and increased blood pressure (55).Somastostin analogues: Octreotide, an octapeptide analogous to somastatin with potent vasoconstrictor action on the splenic vasculature. It acts as an inhibitor of the secretion of peptides synthesized by the gastro-endocrine-pancreatic endocrine system, having the effect of decreasing splenic blood flow (55).Vasopressin analogues: ornipressin, terlipressin. Ornipressin has shown benefits in SHR, but due to its ischemic effects such as arrhythmias, myocardial ischemia and cutaneous necrosis, it has been abandoned. Terlipressin is a synthetic derivative of vasopressin, which has a dominant action on V1 receptors, with a potent vasoconstrictor effect. The administration of volume expanders such as albumin improve the effect of vasoconstrictors (54).
Can an increase in noradrenaline induced by brief exercise counteract sleep inertia?
Published in Chronobiology International, 2020
Katya Kovac, Grace E. Vincent, Jessica L. Paterson, Brad Aisbett, Amy C. Reynolds, Sally A. Ferguson
During an ‘adrenaline rush,’ the sympathetic nervous system mobilizes the body’s resources to fight or flee a threat, triggering a heightened state of alertness (Goldstein 2006). Catecholamines, including adrenaline and noradrenaline, are released from the adrenal glands stimulating several physiological responses. Noradrenaline, for example, is responsible for an increase in heart rate and blood pressure, and the release of stored glucose for energy (Goldstein 2006). Given that sleep inertia is a state of hypo-physiological arousal, the heightened state of physiological alertness experienced during an ‘adrenaline rush’ may counter the impairments to alertness found during sleep inertia. As such, identifying a strategy that can safely and reliably elicit a sympathetic response or ‘adrenaline rush’ may be beneficial for sleep inertia countermeasure research.
Pharmacotherapeutic agents for the management of COVID-19 patients with preexisting cardiovascular disease
Published in Expert Opinion on Pharmacotherapy, 2021
Maryam Khan, Guntaj Kaur Singh, Sakina Abrar, Roshan Ganeshan, Kara Morgan, Amer Harky
In addition, there is also promising evidence that some beta-blockers may also provide a beneficial effect to COVID-19 patients. Patients with COVID-19 can suffer from many clinical changes, including inflammation, due to the SARS-CoV-2 virus’ disruption to the body’s immune system. Beta-2 receptor antagonists could potentially reduce this inflammation and help rebalance the immune system. Moving forward, the beta-2-adrenergic pathway may be further investigated as a possible target to reduce the inflammatory symptoms related to COVID-19. This is thought to be a potential area of interest due to the mechanism of action of beta blockers, which causes a temporary blockade of noradrenaline, diminishing the body’s innate ‘fight or flight’ response. This reduces the stress and therefore workload of the areas in which there are active receptors, such as the vasculature and heart.
Related Knowledge Centers
- Blood Pressure
- Heart Rate
- Organic Compound
- Catecholamine
- Norepinephrine
- Neurotransmitter
- Brain
- Body
- Hormone
- Fight-Or-Flight Response