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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: 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: 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: 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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Related Experiment Video

Updated: Jun 20, 2026

A Convenient Method for Extraction and Analysis with High-Pressure Liquid Chromatography of Catecholamine Neurotransmitters and Their Metabolites
13:35

A Convenient Method for Extraction and Analysis with High-Pressure Liquid Chromatography of Catecholamine Neurotransmitters and Their Metabolites

Published on: March 1, 2018

The catecholamines strike back. What NO does not do.

Michael J Joyner1, Darren P Casey

  • 1Department of Anesthesiology, Mayo Clinic,Rochester, MN 55905, USA. joyner.michael@mayo.edu

Circulation Journal : Official Journal of the Japanese Circulation Society
|September 5, 2009
PubMed
Summary
This summary is machine-generated.

Nitric oxide (NO) plays a limited role in exercise-induced vasodilation in skeletal muscle and skin. Sympathetic nerves can override NO

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Area of Science:

  • Cardiovascular Physiology
  • Endothelial Function
  • Vascular Biology

Background:

  • Endothelial-derived relaxing factor, now known as nitric oxide (NO), is a key regulator of vascular tone.
  • The vascular endothelium is crucial for physiological regulation and pathophysiological dysfunction.
  • Skeletal muscle and skin exhibit significant vasodilation, but underlying mechanisms were unclear.

Observation:

  • Researchers investigated if NO explained unexplained vasodilation in skeletal muscle and skin.
  • The interaction between NO tone and sympathetic tone was examined.
  • The capacity of NO to override sympathetic vasoconstriction was studied.

Findings:

  • NO plays a modest, non-obligatory role in exercise hyperemia and reactive hyperemia.
  • NO is crucial for skeletal muscle vasodilation during mental stress and skin vasodilation during local heating.
  • In animals, NO limits sympathetic vasoconstriction in exercising muscles, but this is not observed in humans.

Implications:

  • NO's role in extreme vasodilation is limited, particularly in skeletal muscle.
  • Sympathetic nerves can modulate vasodilation to maintain arterial blood pressure.
  • Understanding NO and sympathetic interactions is vital for cardiovascular health.