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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...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
Desensitization and Tachyphylaxis01:20

Desensitization and Tachyphylaxis

Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
Several...
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
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...
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...

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Related Experiment Video

Updated: Jun 22, 2026

Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System
06:40

Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System

Published on: May 22, 2018

Acute methamphetamine exposure inhibits cardiac contractile function.

Subat Turdi1, Robbie M Schamber, Nathan D Roe

  • 1Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA.

Toxicology Letters
|June 2, 2009
PubMed
Summary

Methamphetamine directly harms heart muscle function, reducing contractility and calcium handling in cardiomyocytes. This drug abuse impacts cardiac performance and response to adrenergic stimulation, causing protein damage.

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A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
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Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System
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Published on: May 22, 2018

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
09:16

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration

Published on: January 22, 2016

Area of Science:

  • Cardiology
  • Pharmacology
  • Toxicology

Background:

  • Methamphetamine abuse is prevalent, with known cardiovascular risks.
  • The precise mechanisms by which methamphetamine affects cardiac function remain unclear.

Purpose of the Study:

  • To investigate the direct effects of methamphetamine on isolated whole heart and single cardiomyocyte contractile function.
  • To elucidate the impact of methamphetamine on intracellular calcium handling and adrenergic responses in cardiac cells.

Main Methods:

  • Isolated adult FVB mouse hearts and cardiomyocytes were exposed to varying methamphetamine concentrations.
  • Cardiac mechanical function was assessed using Langendorff apparatus and IonOptix Myocam.
  • Western blot analysis examined protein expression (SERCA2a, phospholamban, Na+-Ca2+ exchanger).
  • Cardiomyocyte protein damage was evaluated via carbonyl formation.

Main Results:

  • Methamphetamine depressed left ventricular pressure development (+/-dP/dt), peak shortening (PS), and intracellular Ca2+ rise.
  • The drug blunted norepinephrine-induced positive contractile responses in cardiomyocytes.
  • Upregulation of the Na+-Ca2+ exchanger and cardiomyocyte protein damage (carbonyl formation) were observed.
  • No significant changes in +/-dLdt, TPS, TR(90), resting Ca2+, or Ca2+ decay were noted.

Conclusions:

  • Methamphetamine exerts a direct cardiac depressant effect on both myocardium and isolated cardiomyocytes.
  • Impaired cardiac function may be linked to methamphetamine-induced protein damage and a dampened adrenergic response.
  • Alterations in calcium handling, particularly Na+-Ca2+ exchanger activity, contribute to methamphetamine cardiotoxicity.