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The Scientific Basis of Medicine
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Chris O'Callaghan, Rachel Allen
At their site of action, drugs interact with molecules termed drug ‘receptors’ or ‘targets’. These are often actual biological receptors, such as hormone receptors, but they may also be any other type of molecule, such as an enzyme or membrane channel. The affinity of a drug-receptor interaction is a measure of how tightly the two molecules bind. An agonist is a substance that has an effect on a specific drug receptor, causing activation of the function of the receptor molecule. A partial agonist has the same type of effect on the function of the receptor molecule, but even at the maximal effect of the drug, the function of the receptor molecule is not activated to its maximal level. An antagonist is a drug that binds, to but opposes, the natural activity of the receptor molecule. Competitive antagonists compete with agonists for the same receptor, but they do not exert an agonist effect themselves and so reduce the effect of any agonist present. In these circumstances, the overall effect will depend on the relative concentrations of agonist and antagonist. A non-competitive antagonist does not compete for the same site but opposes the effect of the agonist by another mechanism. Finally, an irreversible antagonist is an antagonist that inactivates the receptor molecule permanently once it has bound. This effect cannot be reversed, even at high concentration of agonist. Many drug receptors are bound by naturally occurring agonists and antagonists, including hormones and neurotransmitters.
The Neuromuscular Junction
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Antagonists of a given neurotransmitter, also referred to sometimes as blockers, are substances that bind to the receptor of the neurotransmitter but reduce or block its action. Antagonists could be competitive, noncompetitive, or uncompetitive. As its name implies, a competitive antagonist competes with the neurotransmitter or agonist for the receptor sites. The binding of the competitive antagonist to the receptor site could be reversible (or surmountable), or it could be irreversible (or insurmountable). In the case of a reversible competitive antagonist, the bond to the receptor site is chemically reversible, so that the blocking action depends on the concentration of the antagonist and is reduced by a higher concentration of the neurotransmitter. On the other hand, increasing the concentration of the neurotransmitter does not reduce the blocking effect of an irreversible competitive antagonist that has bound to the site because the bond of the antagonist to the receptor site is chemically irreversible.
Effects
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
The opposing actions of two or more chemical agents, not necessarily administered simultaneously, are considered to be antagonistic interactions. Different types of antagonism include functional antagonism—the opposing physiological effects of chemicals, such as with central nervous system stimulants versus depressants; chemical antagonism—drugs or chemicals that bind to, inactivate, or neutralize target compounds, such as with the action of chelators in metal poisoning; dispositional antagonism—interference of one agent with the absorption, distribution, metabolism, or excretion (ADME) of another (examples of agents that interfere with absorption, metabolism, and excretion include activated charcoal, phenobarbital, and diuretics, respectively); and receptor antagonism—refers to the occupation of pharmacological receptors by competitive or noncompetitive agents, such as the use of tamoxifen in the prevention of estrogen-induced breast cancer.
N-methyl-D-aspartate receptor antagonists in improving cognitive deficits following traumatic brain injury: a systematic review
Published in Brain Injury, 2022
Moein Khormali, Sama Heidari, Sana Ahmadi, Melika Arab Bafrani, Vali Baigi, Mahdi Sharif-Alhoseini
NMDAR antagonists are divided into three categories: competitive, noncompetitive, and uncompetitive antagonists (10,15). Competitive antagonists, as the name implies, have a competition with the agonist for binding to the agonist binding site (also called classical binding site or orthosteric site). Their effects can be neutralized by increasing the agonist concentration. Selfotel is an example of competitive NMDAR antagonists (16). Noncompetitive antagonists are agents whose effects cannot be neutralized by increasing the agonist concentration. They usually irreversibly bind to a site other than the classical or orthosteric binding site called the allosteric site. Ifenprodil, Eliprodil, Traxoprodil, Ro25-6981, and ethanol are examples of noncompetitive NMDAR antagonists (10). Agents that fall into the third category, uncompetitive antagonists, bind to an internal part of the receptor channel and impede the passage of ions. They are also called channel blockers. Amantadine, dextrorphan, dextromethorphan, dizocilpine, ketamine, magnesium, memantine, and phencyclidine (PCP) fall into this category (10). It should be noted that in some classification schemes, glycine antagonists have been mentioned as a distinct category (15). The reason might be that glycine has sometimes been categorized as an NMDAR modulator rather than an agonist (17).
Combination effect of nanoparticles on the acute pulmonary inflammogenic potential: additive effect and antagonistic effect
Published in Nanotoxicology, 2021
Seonghan Lee, Dong-Keun Lee, Soyeon Jeon, Sung-Hyun Kim, Jiyoung Jeong, Jong Sung Kim, Jong Hyun Cho, Hyuntae Park, Wan-Seob Cho
In this study, the antagonistic effect of CB NPs on the toxicity of metal oxide NPs was evident with the increased inflammatory response and ROS generation potential by decreasing the dose of CB NPs in the combination treatment with NiO NPs. These results suggest that the antagonistic effect of CB NPs is due to the scavenging of ROS that is generated by the CuO or NiO NPs. Carbon-based nanomaterials including carbon nanotubes (CNTs) and CB exert antioxidant effects in vivo and in vitro by scavenging ROS (Watts et al. 2003; Fenoglio et al. 2006; Crouzier et al. 2010; Nymark et al. 2014). Thus, CNTs and graphene can deplete cellular antioxidant enzymes through the oxidation of glutathione using the oxygen on the surface of CNTs (Liu et al. 2011). As the oxidative stress caused by CNTs could be due to metal impurities (e.g. iron), which can increase the free radicals via the Fenton reaction, we can infer that the high purity CNTs and CB NPs can have a superior ROS scavenging effect, which can mitigate the toxicity of metal oxide NPs (Kagan et al. 2006). In addition, the high binding affinity of CB NPs to biomolecules than most of metal oxide NPs can be another contributor to the antagonistic effect (Kroll et al. 2012; Lee et al. 2015). However, more studies are needed to define the type of antagonism observed in this study.
Antibiotic combination therapy against resistant bacterial infections: synergy, rejuvenation and resistance reduction
Published in Expert Review of Anti-infective Therapy, 2020
Anthony R. M. Coates, Yanmin Hu, James Holt, Pamela Yeh
Using multiple drugs at once can also have either synergistic or antagonistic effects which, depending on requirements, can both be useful [27,34,38,72]. Antagonism occurs when drug interactions produce an overall effect less than the sum of the individual drugs, leading to an attenuated effect [72]. Synergistic antibiotic combinations lead to more effective killing of bacteria and can rejuvenate antibiotics to which resistance has developed, but select more for resistance [27,34,38,72]. Synergistic combinations can also lead to a reduction in the dose of a toxic antibiotic which means that patients will have less side-effects from treatment. Antagonistic combinations produce less selection pressure but are less bactericidal [99,100]. The adverse effects of combination therapy should be tested in both pre-clinical and clinical trials.