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Related Concept Videos

Indirect-Acting Cholinergic Agonists: Mechanism of Action01:18

Indirect-Acting Cholinergic Agonists: Mechanism of Action

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Indirect-acting cholinergic agonists work by interacting with an enzyme called acetylcholinesterase (AChE) in the synaptic cleft. They can be reversible or irreversible inhibitors and have different effects on the enzyme.
Reversible inhibitors like edrophonium bind to a specific part of the enzyme called the anionic catalytic site. They form noncovalent bonds, which means they are not strongly attached to the enzyme. This creates a temporary and less stable enzyme–inhibitor complex,...
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Direct-Acting Cholinergic Agonists: Pharmacokinetics01:31

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Direct-acting cholinergic agonists, such as synthetic choline esters and naturally occurring alkaloids, exert their effects by enhancing the actions of acetylcholine and stimulating the parasympathetic nervous system. Synthetic choline esters share structural similarities with acetylcholine. For example, they have a positively charged quaternary ammonium or onium group, contributing to their hydrophilic characteristics. As a result, they are poorly absorbed in the body through oral...
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Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:22

Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship

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Cholinergic agonists or cholinomimetics mimic the action of acetylcholine to stimulate the parasympathetic nervous system. They are categorized into direct-acting and indirect-acting agents. The direct-acting cholinergic drugs induce the parasympathetic response by directly binding to the muscarinic or nicotine receptors. In comparison, the indirect-acting cholinergic drugs prevent acetylcholine hydrolysis, indirectly contributing to the extended parasympathetic response.
The direct-acting...
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Indirect-Acting Cholinergic Agonists: Pharmacological Actions01:30

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Indirect-acting cholinergic agonists, also known as anticholinesterases, exert their pharmacological effects by enhancing cholinergic transmission in various body parts, including the neuromuscular junction, autonomic cholinergic synapses, and the brain.
At the neuromuscular junction, these agents work by inhibiting the breakdown of acetylcholine, allowing it to remain bound to the receptor and bind to nearby receptors. This process leads to repetitive firing of the endplate, causing muscle...
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Indirect-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:29

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Indirect-acting cholinergic agonists are agents that interact with the acetylcholinesterase enzyme in the synaptic cleft, preventing the breakdown of acetylcholine into choline and acetate. Consequently, the concentration of acetylcholine in the synaptic cleft increases. These agonists can be classified into reversible and irreversible inhibitors based on their duration of action.
Reversible inhibitors display short to medium durations of action. Short-acting agents include simple alcohols with...
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Depolarizing Blockers: Mechanism of Action01:28

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Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
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Related Experiment Video

Updated: Mar 6, 2026

Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders
06:39

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Ultra-long acting calcium channel blockers may decrease accuracy of the acetylcholine provocation test.

Manabu Kurabayashi1, Mitsutoshi Asano1, Tsukasa Shimura1

  • 1Division of Cardiology, Yokohama City Minato Red Cross Hospital, Yokohama, Japan.

International Journal of Cardiology
|March 8, 2017
PubMed
Summary

A 48-hour washout for calcium channel blockers (CCBs) before coronary spasm tests may be insufficient. Ultra-long acting CCBs like amlodipine can reduce test sensitivity, suggesting a longer drug holiday is needed.

Keywords:
Acetylcholine provocation testCalcium channel blockerCoronary artery spasmCoronary artery tone

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Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Standard practice recommends a >48h washout for calcium channel blockers (CCBs) before coronary spasm provocation tests.
  • The distinct half-lives of CCBs and their impact on acetylcholine provocation tests are not well understood.

Purpose of the Study:

  • To investigate the influence of prior oral calcium channel blocker (CCB) administration on the acetylcholine provocation test for evaluating coronary vasomotor reactions.

Main Methods:

  • Examined 245 patients with suspected vasospastic angina undergoing acetylcholine provocation tests.
  • Compared outcomes for patients on amlodipine (ultra-long acting CCB), other CCBs, and no CCB, after a >48h drug withholding period.

Main Results:

  • Patients on amlodipine showed lower coronary artery tone and a reduced positive acetylcholine provocation test rate (41%) compared to other CCBs (68%) and no CCB (64%).
  • Multivariate analysis identified amlodipine use up to 2 days prior as an inverse predictor of acetylcholine-provoked coronary spasm (OR 0.327, p=0.023).

Conclusions:

  • Residual vasodilatory effects of ultra-long acting CCBs may blunt coronary artery tone and reduce vasoconstrictive response to acetylcholine.
  • A 2-day pre-test drug holiday may be inadequate for ultra-long acting CCBs, potentially affecting diagnostic accuracy for coronary spasm.