Nature and chemical structure of atropine
Atropine is an alkaloid naturally derived from plant sources. The main natural sources of this compound include plants such as deadly nightshade (also known as belladonna) and henbane.
The ability of atropine to interfere with the nervous system is directly dependent on its chemical structure. The drug molecule has a pronounced structural similarity to the endogenous neurotransmitter acetylcholine. Specifically, the structure of atropine contains an ester group and a nitrogen-containing moiety. It is precisely this match of functional groups and their specific spatial arrangement that allows the drug molecule to successfully compete with acetylcholine for binding sites on receptors.
Mechanism of action and effects of atropine
According to its mechanism of action, atropine is a specific competitive inhibitor of M-cholinergic receptors. It physically blocks the binding of acetylcholine molecules to these receptors.
The main pharmacological effect of this blockade is its action on the smooth muscle of internal organs. By preventing smooth muscle contraction, atropine causes profound relaxation, acting as a potent antispasmodic.
The clinical application of the drug is based on this effect:
- In ophthalmology, it is used for the targeted relaxation of intraocular muscles, which is necessary for a physician to properly examine the patient's fundus.
- In gastroenterology, the drug is indispensable for relieving acute spasms associated with gastrointestinal colic.
Adverse effects of high doses of atropine
When the drug is used in high doses, there is a risk of serious adverse effects. Primarily, these are associated with the penetration of the substance into the central nervous system and its action on M-cholinergic receptors located there.
The main manifestations of the toxic action of high doses include:
- Severe motor agitation;
- Psychological agitation;
- Appearance of hallucinations;
- Onset of seizures.
Suxamethonium: a curare-like muscle relaxant
Unlike atropine, suxamethonium affects a different group of receptors and is a competitive agonist of N-cholinergic receptors. It belongs to the group of curare-like drugs — a term historically applied to muscle relaxants after such properties were first discovered in the indigenous arrow poison curare.
The site of action of suxamethonium is exclusively the neuromuscular junctions of skeletal muscles, which are rich in N-cholinergic receptors. The drug is also a structural analogue of acetylcholine and is capable of binding directly to the receptors.
Mechanism of persistent depolarization
Despite the fact that suxamethonium binds to receptors similarly to acetylcholine, its degradation in the synaptic cleft occurs differently. The process of muscle relaxation takes place in several stages:
- The drug binds to N-cholinergic receptors.
- Unlike the endogenous neurotransmitter, suxamethonium is degraded very slowly by a specialized enzyme, acetylcholinesterase.
- Due to the prolonged presence of the substance in the synapse, ion channels remain open for an extended period, causing persistent membrane depolarization.
- As a consequence, nerve impulse conduction is completely disrupted, leading to profound muscle relaxation.
This specific effect is widely used in medical practice during surgical operations and complex endoscopic procedures where complete relaxation of the patient's skeletal musculature is required.
Briefly: answers to topical questions
What antidotes are used in atropine poisoning?
In atropine overdose, acetylcholinesterase inhibitors are used as antidotes.
Since atropine is a competitive inhibitor, increasing the concentration of the substrate in the synaptic cleft allows it to be displaced from its bond with the receptor. Drugs of this group include:
- Physostigmine — an acetylcholinesterase inhibitor that blocks the breakdown of the endogenous neurotransmitter.
- Neostigmine — an acetylcholinesterase inhibitor that promotes the accumulation of endogenous acetylcholine.
What are the main contraindications to the use of atropine?
The main contraindications to the drug logically stem from its adverse effects.
These include:
- Glaucoma — the drug increases intraocular pressure.
- Benign prostatic hyperplasia — there is a risk of acute urinary retention.
- Cardiovascular pathologies — presence of tachyarrhythmias.
- GI pathologies — intestinal atony.
How does atropine affect exocrine gland secretion?
Atropine decreases salivary and bronchial gland secretion; this effect is utilized in anesthesiology for premedication prior to general anesthesia.
Additionally, M-anticholinergics, which include atropine, are associated with dry mucous membranes and skin.
Class and exam questions
Why is atropine able to bind to receptors instead of acetylcholine?
This is due to their chemical affinity. Atropine has an ester group and a nitrogen-containing fragment, and the spatial arrangement of its functional groups matches the structure of acetylcholine.
What is the difference between the mechanism of action of atropine and suxamethonium?
Atropine is an M-cholinergic receptor inhibitor and induces smooth muscle relaxation. Suxamethonium acts as an N-cholinergic receptor agonist and relaxes skeletal muscle.
How does suxamethonium block nerve impulse conduction if it acts like acetylcholine?
Upon binding to the receptor, suxamethonium is broken down very slowly by the enzyme acetylcholinesterase. This leads to prolonged opening of ion channels and persistent membrane depolarization, making the conduction of new impulses impossible.
Why is an atropine overdose dangerous?
In high doses, the drug begins to block M-cholinergic receptors in the central nervous system. This leads to psychological and motor agitation, hallucinations, and seizures.
What else to study on this topic
- Structural formulas of atropine and acetylcholine: comparison of functional groups
- Differences between M-cholinergic and N-cholinergic receptors in terms of body localization
- The role of the enzyme acetylcholinesterase in neuromuscular junctions
- Mechanism of action of curare-like drugs
- The process of membrane depolarization and the function of ion channels
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