Main Question Post This post will describe agonists, antagonists, and partial ag

Main Question Post
This post will describe agonists, antagonists, and partial agonists. Also, g couple proteins and ion-gated channels will be compared and discussed. Lastly, epigenetic mechanisms will be described, and all of these will be discussed in their relevance to prescribing medications in clinical practice.
The Agonist-to-Antagonist Spectrum of Action
Antagonists block the binding of endogenous molecules to cell receptors. They have high affinity but low intrinsic activity. This means that they will readily occupy a receptor but block the typical reaction that the receptor would cause. Antagonists only work in the presence of agonists or endogenous molecules seeking to bind with receptors. For example, taking Narcan in the absence of opiates will have no effect. Antagonists are competitive and noncompetitive. Competitive antagonists only exert an effect when they outnumber the agonist. Conversely, noncompetitive antagonists occupy the receptor permanently until the receptor is replaced. This causes the effect to be more prolonged because total receptor capacity has been temporarily reduced (Rosenthal & Burchum, 2021).
Agonists mimic the effects of endogenous molecules. They have a high affinity for receptors and also high intrinsic activity. This means that they will produce the same effect as the endogenous molecules. Partial agonists have affinity for receptors but only relative intrinsic activity. This means that they operate as agonists and antagonists. They act as agonists because of the intrinsic activity they produce. As antagonists, they block the receptor site for other molecules that may have higher intrinsic activity, thus limiting the total intrinsic effect of the cell. This can be used when a maximal response from a medication is not the desired outcome (Rosenthal & Burchum, 2021).
Ion-gated Channels Vs. G Couple Proteins
G couple proteins and ion-gated channels are both ways cells communicate with their outside environments. Ion channels cause a rapid influx of ions into the cell. In neurons, this produces action potentials. The rapid influx of ions allows the rapid polarization and depolarization of neurons. Effects from ion channels are brief and relatively uncomplicated.
On the other hand, g couple proteins cause slower, more sustained responses. They operate not by opening channels for ions but via second messenger systems. These often involve a cascade of reactions using several enzymes. The cascade results in some kind of modification within the cell via triggering proteins to perform a variety of functions, including manufacturing neurotransmitters, and adjusting cytoskeletal arrangements, amongst many others (Camprodon & Roffman, 2016).
The Role of Epigenetics in Pharmacologic Actions
Epigenetic changes can occur without mutation of the DNA code, and there is evidence that alteration may be heritable. This means that medications that help biological parents may be helpful to their offspring. Treatments using epigenetic principles are still in development. Valproic acid, commonly used for bipolar disorders, appears to operate via epigenetic principles (Camprodon & Roffman, 2016).
A common example of epigenetics comes from Adverse Childhood Event (ACE) scores. A child with high ACE scores is not only affected by the trauma and behavioral learning of their caregivers, but they are also more likely to develop a chronic disease like COPD, liver disease, and ischemic heart disease. The clinical relevance here is that patients with high ACE scores are likely to respond differently or unfavorably to treatment that would produce a result in others. Epigenetics can also function in the opposite direction. If given enough support, a person with severe mental illness can prevent passing on epigenetic burdens to their offspring (Van Der Kolk, 2015).
Clinical Relevance
Often patients will want to be prescribed the medication that is the “best” or “most potent.” This shows a misunderstanding of the balance struck in pharmacology. Sometimes it is pertinent to produce an effect that is not a maximal effect. Also, prescribing an agonist along with a partial agonist might produce a reduced effect. In this way, being on multiple medications is not ideal. If agonists share receptors, they will compete, and the one with the highest affinity will bind with the receptor. This potentially gives the patient the benefit of only one medication while exposing them to the systemic adverse effects of both. Lastly, epigenetics emphasizes the importance of taking a thorough family history and providing adequate psychosocial support along with medication treatment.
References
Camprodon, J. A., & Roffman, J. L. (2016). Psychiatric neuroscience: Incorporating pathophysiology into clinical case formulation. In T. A. Stern, M. Favo, T. E. Wilens, & J. F. Rosenbaum. (Eds.), Massachusetts General Hospital psychopharmacology and neurotherapeutics. Elsevier.
Rosenthal, L. D., & Burchum, J. R. (2021). Lehne’s pharmacotherapeutics for advanced practice nurses and physician assistants (2nd ed.) St. Louis, MO: Elsevier.
Van Der Kolk, B., MD. (2015). The Body Keeps the Score: Brain, Mind, and Body in the Healing of Trauma. National Geographic Books.
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