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Immunoregulation By Pituitary Hormones
Published in Istvan Berczi, Pituitary Function and Immunity, 2019
Lymphocytes, granulocytes and mast cells have β -2-type catecholamine receptors, whereas platelets express α -type receptors. Catecholamines appear to have major influences on leukocyte recirculation and distribution, some of which is mediated through the ACTH-corticosteroid axis.42 It is somewhat hazardous to draw conclusions from studies with synthetic catecholamine receptor agonists and antagonists. Nevertheless, it seems reasonably certain that β -adrenergic stimulants stabilize mast cells in several species (mouse, rat, man), inhibit mediator release, and thus, decrease the sensitivity to asthma and allergic reactions. The reaction of murine and human lymphocytes to mitogens (Con A, PHA, PWM, LPS) is also inhibited by catecholamines. Humoral and cell mediated immune reactions in mice are in general inhibited, although some agents seem to cause acceleration and enhancement. Immunoglobulin synthesis by human peripheral blood lymphocytes is enhanced by catecholamines and further amplified by glucocorticoids. The maturation of human neutrophils is inhibited by adrenergic agents. Thus, the effect of β -adrenergic agents on the immune system in general, and on allergic-asthmatic reactions in particular, seems to be inhibitory, although occasional acceleration and enhancement was also observed. Additional observations are needed for further clarification of the effect of catecholamines on the immune system.
Drug Targeting to the Lung: Chemical and Biochemical Considerations
Published in Anthony J. Hickey, Sandro R.P. da Rocha, Pharmaceutical Inhalation Aerosol Technology, 2019
Peter A. Crooks, Narsimha R. Penthala, Abeer M. Al-Ghananeem
Another strategy for obtaining an enhancement in pulmonary clearance of drugs is to conjugate the drug molecule to a chemical entity that binds to one or more surface receptors on endothelial or epithelial cells. Examples of the receptor agonists serotonin and norepinephrine have already been mentioned. However, there are examples of lung targeting that have used other pulmonary receptor substrates as targeting vectors (Geiger et al. 2010, Vallath et al. 2014, Korbelin et al. 2016, Orriols et al. 2017).
Sedation and analgesia
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Anesthesia for Neurotrauma, 2018
Paola Cristina Volpi, Barbara Cambiaghi, Giuseppe Citerio
Opioids are the natural chemical derivatives of opium. They act as µ-opioid receptor agonists that produce a variety of effects, including analgesia, sedation, bradycardia, respiratory depression, nausea, and pruritus. They reinforce the effects of sedatives when used in combination, but do not cause amnesia when used alone.
How can we improve the measurement of receptor signaling bias?
Published in Expert Opinion on Drug Discovery, 2023
Furthermore, it is therapeutically essential to distinguish ‘partial’ from ‘biased’ receptor agonists. A number of recent studies showed that the improved side effect profile of some ligands could be explained by their low efficacy at stimulating the receptor (partial agonism), and not necessarily because of their greater efficacy for activating a specific signaling pathway over another (signaling bias) [14,17]. However, despite all efforts in refining our approaches for predicting the therapeutic effect of biased agonists using simple cellular responses, failures in the clinic should be expected as additional levels of translational testing that associate in vivo responses with specific in vitro signaling effects might be required. This, however, should not diminish our interest in bias signaling as a viable therapeutic approach in drug discovery.
An overview of the pharmacotherapeutics for dystonia: advances over the past decade
Published in Expert Opinion on Pharmacotherapy, 2022
O. Abu-hadid, J. Jimenez-Shahed
A critical gap remains in the treatment of generalized and hemidystonia as well as some forms of segmental dystonia, where botulinum toxin treatment alone may be insufficient due to dosing limitations. Oral medications are often used in combination with injections to improve symptoms to a greater extent. While helpful, they are often associated with dose-limiting side effects such as drowsiness and cognitive impairment due to their generally inhibitory effect on the central nervous system. Furthermore, they are not targeted to exactly address the underlying pathology. Fortunately, some forms of genetic dystonias can be treated with oral medications such as in the case of dopa-responsive dystonia. However, in refractory cases, DBS or ITB should be considered. With the growing understanding of the proposed network model of dystonia, novel stimulation targets or methods may be considered. Additionally, the ongoing development of animal models which may better represent dystonia heterogeneity will facilitate testing of novel experimental therapeutics, as well as discovery of additional relevant and modifiable biochemical pathways [141]. Examples may include drugs selective for particular receptor subtypes that may yield improved tolerability, such as with muscarinic acetylcholine receptor antagonists, or those which use different pathways to modulate striatial dopaminergic transmission, such as nicotinic receptor agonists.
A mechanistic evaluation of the potential for octamethylcyclotetrasiloxane to produce effects via endocrine modes of action
Published in Critical Reviews in Toxicology, 2021
In order for a chemical to act as a receptor agonist it must be capable of binding in the agonist binding site of its receptor and stimulating (activating) the receptor once bound. Receptor antagonists must be capable of binding to the receptor and interfering with the ability of the receptor to be stimulated by its agonist. Binding between receptors and their agonists or antagonists and the ability of the agonist to stimulate the receptor require that the two molecules “fit” together with very precise interactions. These include high degrees of specificity for size, shape, charge, and chemical properties. Co-activators, co-repressors, agents that interfere with transport or storage of receptor agonists or antagonists, and substances that act to enhance metabolic breakdown of receptor agonists or antagonists, are indirect secondary effects that do not meet the U.S. EPA criteria for evaluation as potential endocrine disruptors.