What is the action of acetylcholine and anticholinesterase. Confused

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Discussion Overview

The discussion revolves around the actions of acetylcholine and anticholinesterase, particularly focusing on the effects of increased acetylcholine levels in the body, the implications for sympathetic and parasympathetic activity, and the clinical effects of anticholinesterase poisoning. Participants explore both theoretical and practical aspects of these interactions.

Discussion Character

  • Exploratory
  • Technical explanation
  • Debate/contested

Main Points Raised

  • One participant states that acetylcholine is released from postganglionic parasympathetic fibers and preganglionic nerve fibers of both sympathetic and parasympathetic nerves, causing muscle contraction at the neuromuscular junction.
  • Another participant notes that high acetylcholine levels would be present at the end organ level rather than at the junction, suggesting that the effects may differ based on location.
  • There is a question about whether increased acetylcholine in preganglionic sympathetic fibers would also enhance sympathetic activity, leading to uncertainty about the final effects.
  • Concerns are raised regarding the clinical effects of anticholinesterase poisoning, with references to symptoms such as pupillary constriction and bronchoconstriction.
  • A participant inquires about the interaction between anticholinesterase and competitive agonists or neuromuscular blocking agents, questioning if it would decrease the action of such agents due to increased acetylcholine levels.
  • Another participant mentions that acetylcholine's half-life is short, which may affect its concentration at nerve junctions compared to end organs.

Areas of Agreement / Disagreement

Participants express uncertainty regarding the overall effects of increased acetylcholine levels, particularly in relation to sympathetic activity. There is no consensus on the final outcomes or the implications of anticholinesterase use in combination with other agents.

Contextual Notes

Participants highlight the complexity of acetylcholine's actions and the potential for varying effects based on its concentration at different sites in the body. The discussion reflects a need for clarity on the mechanisms involved and the clinical implications of anticholinesterase use.

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What is the action of acetylcholine and anticholinesterase. Confused!

Hello everyone,

Ok Acetylchlone is released from postganglionic parasympathetic fibres and preganglionic nerve fibres of both sympathetic and parasympathetic nerves. It also cause muscle contraction in neuromuscular junction. So anticholinesterase would increase acetylcholine level---> Now what would be the effects of increased acetylcholine. Ok I understand parasympathetic activity would be increased, but if lots of acetylcholine is there in preganglionic nerve fibres of sympathetic fibres now, shouldn't sympathetic activity also increase. So what is the final effect.Also in anticholinesterase poisoning what are the clinical effects. I can't work it out because of my previous confusion. Is is like pupillary constriction and bronchoconstriction if parasympathetic predominates. Also increased muscle contraction. Also if I use anticholinesterase in combination with a competitive agonist and neuromuscular blocking agent such as tubocurarine would this decrease the action of tubercurine, because now it has compete with acetylcholine.

Thanks for help in advance :smile:
 
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first high acetylcholine levels would be at the end organ level, not junction.

The effects of overdose is exactly like you said, plus a couple of other ones you can probably find onlline
 


mazinse said:
first high acetylcholine levels would be at the end organ level, not junction.

The effects of overdose is exactly like you said, plus a couple of other ones you can probably find onlline

Hey thanks for taking your time to help :smile: But could u please elaborate when you say "first high acetylcholine levels would be at the end organ level, not junction." Does this mean that if i give a cholinergic drugs (acetylcholine agonists), they will travel through the blood stream and reach the organs first, so by the time they reach nerve junctions there concentration would be very low hence minimum sympathetic activity.
 


yeah that's what i am thinking, especially since acetylcholine's half life isn't that long to begin with.
 

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