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Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

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Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which...
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Adrenergic Antagonists: Chemistry and Classification of ɑ-Receptor Blockers01:17

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Adrenergic antagonists, or sympatholytics, inhibit adrenoceptor activation driven by catecholamines or agonists. Based on their adrenoceptor specificity, adrenergic blockers can be categorized into two primary groups: α-adrenergic blockers (α-blockers) and β-adrenergic blockers (β-blockers). α-blockers interact with α1 and α2 subtypes of α-adrenoceptors.
Nonselective α-blockers: Nonselective α-blockers contain haloalkylamine or imidazoline...
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Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

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Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral...
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Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
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Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

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Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of...
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Adrenergic Agonists: Direct-Acting Agents01:30

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Drugs that mimic the action of endogenous catecholamines like noradrenaline and adrenaline are called adrenergic agonists or sympathomimetics. Based on their mechanism of action, sympathomimetics can be classified as direct-, indirect-, or mixed-acting sympathomimetics. Direct-acting adrenergic agonists activate adrenoceptors without affecting presynaptic neurons, making them independent of neuronal catecholamine-depleting agents like reserpine and guanethidine.
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HPLC-based Assay to Monitor Extracellular Nucleotide/Nucleoside Metabolism in Human Chronic Lymphocytic Leukemia Cells
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Drugs targeting adenosine signaling pathways: A current view.

Barbara Kutryb-Zając1, Ada Kawecka1, Khrystyna Nasadiuk1

  • 1Department of Biochemistry, Medical University of Gdańsk, 80-211 Gdańsk, Poland.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|July 28, 2023
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Adenosine signaling pathways are crucial for health and disease. Targeting these pathways offers therapeutic potential for various conditions, enabling drug repurposing and new treatment strategies.

Keywords:
AdenosineCancerCardiovascular diseasesDrugsNeurodegeneration

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Area of Science:

  • Pharmacology
  • Biochemistry
  • Molecular Biology

Background:

  • Adenosine, an endogenous nucleoside, regulates physiological and pathological processes via G-protein-coupled receptors.
  • It protects tissues during high metabolism and prevents organ dysfunction in disease.
  • Modulating adenosine pathways is a potential therapeutic strategy for numerous human diseases.

Purpose of the Study:

  • To review pharmaceuticals and tools targeting adenosine signaling.
  • To summarize FDA-approved and investigational drugs affecting adenosine pathways.
  • To actualize current knowledge on adenosine signaling in therapeutics.

Main Methods:

  • Literature review of drugs targeting adenosine signaling.
  • Inclusion of FDA-approved drugs and clinical trial candidates.
  • Analysis of drugs with primary or secondary adenosine pathway modulation.

Main Results:

  • Identified A2A adenosine receptor modulators (e.g., istradefylline, regadenoson).
  • Cataloged anti-platelet, anti-inflammatory, immunosuppressive, and anti-cancer drugs impacting adenosine signaling.
  • Highlighted numerous adenosine pathway regulators in clinical trials for infectious and noninfectious diseases.

Conclusions:

  • Targeting purinergic signaling presents significant therapeutic opportunities.
  • Understanding adenosine's role in drug mechanisms facilitates drug repurposing.
  • Adenosine pathway modulation opens avenues for novel therapeutic strategies.