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Related Concept Videos

Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

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 bioavailability, and...
Adrenergic Agonists: Mixed-Action Agents01:28

Adrenergic Agonists: Mixed-Action Agents

Mixed-action adrenergic agonists, like ephedrine and pseudoephedrine, directly and indirectly affect adrenergic receptors. These agents stimulate adrenoceptors and indirectly release stored neurotransmitters, amplifying the adrenergic response.
Ephedrine and pseudoephedrine lack a catecholamine group, making them less susceptible to degradation by metabolic enzymes. They have increased oral bioavailability and lipophilicity, resulting in a longer duration of action. Their response is reduced by...
Adrenergic Agonists: Direct-Acting Agents01:30

Adrenergic Agonists: Direct-Acting Agents

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.
These agents can be classified...
Adrenergic Neurons: Neurotransmission01:27

Adrenergic Neurons: Neurotransmission

Postganglionic sympathetic fibers (except those supplying the sweat glands) releasing noradrenaline or norepinephrine are called noradrenergic or adrenergic neurons. Noradrenaline, dopamine, adrenaline, or epinephrine are collectively called "catecholamines" as they contain a catechol moiety and an amine side chain. The five stages of neurotransmitter release involve their synthesis, storage, release, reuptake and metabolism.
Synthesis: Catecholamine synthesis requires tyrosine, which is taken...
Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

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...
Adrenergic Agonists: Therapeutic Uses01:30

Adrenergic Agonists: Therapeutic Uses

Adrenergic agonists have diverse therapeutic uses across various medical conditions and emergencies.
Emergency and Intensive Care Unit (ICU) applications: Pressor agents increase blood pressure, heart rate, and contractility in shock and organ failure situations. Dopamine can induce vasodilation and stimulate adrenoceptors. Endogenous catecholamines are effective in treating cardiogenic shock. α2-agonists like clonidine can reverse anesthesia-induced hypertension.
Allergies and anaphylaxis:...

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Caffeine Extraction, Enzymatic Activity and Gene Expression of Caffeine Synthase from Plant Cell Suspensions
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Caffeine Extraction, Enzymatic Activity and Gene Expression of Caffeine Synthase from Plant Cell Suspensions

Published on: October 2, 2018

Caffeine and adenosine.

Joaquim A Ribeiro1, Ana M Sebastião

  • 1Institute of Pharmacology and Neurosciences, Faculty of Medicine and Unit of Neurosciences, Institute of Molecular Medicine, University of Lisbon, Lisbon, Portugal. jaribeiro@fm.ul.pt

Journal of Alzheimer'S Disease : JAD
|February 19, 2010
PubMed
Summary

Caffeine primarily works by blocking adenosine receptors (ARs) in the brain, impacting functions like sleep and cognition. This mechanism offers potential therapeutic strategies for various neurological disorders.

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Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • Caffeine exerts biological effects mainly through antagonizing adenosine receptors (ARs).
  • Adenosine receptors are present in neurons and glial cells across all brain areas.
  • Caffeine's antagonism of ARs opposes the effects of endogenous adenosine.

Purpose of the Study:

  • To elucidate the multifaceted biological actions of caffeine beyond adenosine receptor antagonism.
  • To explore caffeine's impact on normal brain functions and its potential in treating brain dysfunctions.
  • To highlight the therapeutic potential of targeting adenosine receptors with caffeine.

Main Methods:

  • Review of existing literature on caffeine's pharmacological actions.
  • Analysis of caffeine's effects on adenosine receptor subtypes (A1, A2A, A3, A2B).
  • Examination of caffeine's influence on other cellular targets like phosphodiesterases and GABA-A receptors.

Main Results:

  • Caffeine antagonizes all four adenosine receptor subtypes.
  • Additional actions include phosphodiesterase inhibition, calcium release, and GABA-A receptor interference.
  • Caffeine influences cognitive functions, sleep, learning, and memory.

Conclusions:

  • Caffeine's antagonism of adenosine receptors is key to its effects on brain function and dysfunction.
  • Targeting adenosine receptors with caffeine shows promise for treating neurological conditions.
  • Caffeine's broad actions present therapeutic opportunities for brain disorders like Alzheimer's, Parkinson's, and depression.