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Nonopioid and Adjuvant Analgesic Agents
Published in Pamela E. Macintyre, Stephan A. Schug, Acute Pain Management, 2021
Pamela E. Macintyre, Stephan A. Schug
Alpha-2-adrenoreceptors (or α2-receptors) are located on peripheral sensory nerve terminals and in the spinal cord and brain stem. While the mechanisms and relevance of the peripheral and supraspinal effects continue to be debated, the spinal effects are well described. Peripherally and centrally, α2-agonism has an inhibitory effect on pain transmission. Endogenous activation is by norepinephrine (noradrenaline), which explains some of the analgesic effect of norepinephrine reuptake inhibitors such as tramadol and antidepressants. These receptors in the spinal cord are thought to be primarily responsible for the analgesic effects of α2-adrenergic agonists such as clonidine and dexmedetomidine (Giovannitti et al, 2015). Alpha-2-adrenergic agonists are usually used in combination with other analgesic medicines such as local anesthetics or opioids.
Paper 4: Answers
Published in Sabina Burza, Beata Mougey, Srinivas Perecherla, Nakul Talwar, Practice Examination Papers for the MRCPsych Part 1, 2018
Sabina Burza, Beata Mougey, Srinivas Perecherla, Nakul Talwar
False. It does so by acting as an antagonist at alpha2 receptors, resulting in increased norepinephrine release. It is also an alpha1, 5HT2A and M1 antagonist. (10: p.690)
Brain protection
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Manual of Neuroanesthesia, 2017
Judith Dinsmore, Rebecca Campbell
Alpha-2 agonists, such as dexmedetomidine, have emerged in recent years as an alternative for sedation, analgesia, and anesthesia with the potential to attenuate excitotoxic brain injury. Their sympatholytic properties have been proposed as a potential neuroprotective mechanism through a reduction in free radicals, reduced sensitivity to excitatory amino acids such as glutamate, and improvement in both perfusion of the ischemic penumbra, and balance of oxygen supply with demand. However, there have also been concerns from animal models that any reduction in CBF may be out of proportion with decreases in CMR, potentially putting vulnerable neuronal tissue at risk.9 Further clinical trials are required to elucidate the use of alpha-2 agonists in clinical practice.
Histopathological evaluation of the effects of dexmedetomidine against pituitary damage ınduced by X-ray irradiation
Published in Biomarkers, 2023
Filiz Mercantepe, Levent Tumkaya, Tolga Mercantepe, Sema Rakici
Dexmedetomidine is a highly selective alpha-2 (α2) adrenergic agonist that is widely used in sedation and anaesthesia (Qiu et al.2020). Alpha-2 receptors are found in various organs including the liver, lungs, kidneys, and brain. Dexmedetomidine appears to reduce renal inflammation and ischaemia-reperfusion injury based on animal studies (Boersma et al.1996). Several studies have suggested that it has anti-inflammatory effects in cases of brain damage due to various causes (Su et al.2016, Qiu et al.2018). Animal studies have shown that it can potentially offer protection against neuro-apoptosis induced by other agents and that it has neuroprotective and cardioprotective effects (Defraene et al.2017, Stam et al.2019, Schlaak et al.2020). Moreover, animal models of induced cerebral ischaemia and reperfusion determined improved neurological outcomes and reduced cerebral necrosis (Ghita et al.2020). These neuroprotective qualities are thought to arise from reduced cerebral catecholamine and glutamate release and the modulation of apoptosis-regulatory proteins (Stam et al.2017). Therefore, in this study, we aimed to investigate the potential negative effects of x-ray radiation and the effects of the α2-adrenergic receptor agonist dexmedetomidine on the pituitary gland using histopathological and immunohistochemical methods.
Sublingual dexmedetomidine: repurposing an anesthetic as an anti-agitation agent
Published in Expert Review of Neurotherapeutics, 2023
Justin Faden, Meghan Musselman, Leslie Citrome
The alpha-2-adrenergic receptor is an autoreceptor that regulates the release of norepinephrine. Excess norepinephrine is a contributor to hyperarousal states such as agitation and panic. There are three subtypes of the alpha-2 adrenergic receptor, alpha-2A, alpha-2B, and alpha-2C, with alpha-2A being predominant in the locus coeruleus, a region of the brain associated with the arousal system [43,44]. Several alpha-2 adrenergic receptor agonists are currently available including clonidine, dexmedetomidine, guanfacine, and lofexidine. Of these options, dexmedetomidine has the highest affinity and highest intrinsic action on the alpha-2A receptor, thereby perhaps better positioned to ameliorate hyperarousal states[27]. Additionally, although dexmedetomidine is more sedating than clonidine due to greater selectivity for alpha 2 receptors than alpha 1 receptors (A2:A1 ratio 1620:1 vs 220:1), an important attribute of dexmedetomidine-based sedation is that patients remain easily arousable [45,46].
Current and emerging pharmacotherapeutic strategies for Tourette syndrome
Published in Expert Opinion on Pharmacotherapy, 2022
The pharmacological activity of alpha-2 agonists is directed against adrenergic neurotransmission, with clinically significant effects at the level of the sympathetic nervous system, which seems to be involved in the pathophysiology of TS [22,60,61]. Both clonidine and guanfacine bind to alpha-2 adrenergic receptors at pre-synaptic level, resulting in decreased release of noradrenaline. The systemic effects of alpha-2 agonists are responsible for their known anti-hypertensive effects. Alpha-2 agonists have long been used for the treatment of both tics and behavioral symptoms, ranging from attention-deficit and hyperactivity disorder to irritability. Specifically, clonidine and guanfacine have been shown to be effective as non-stimulant pharmacotherapy for attention-deficit and hyperactivity disorder, and are therefore more commonly used in younger patients with TS and this common co-morbidity [62]. There is also evidence that the effect size of alpha-2 agonists on tic reduction is considerably larger in patients who have both TS and co-morbid attention-deficit and hyperactivity disorder, as compared to patients with TS without attention-deficit and hyperactivity disorder [63].