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(əsēt'əlkō`lēn), a small organic molecule liberated at nerve endings as a neurotransmitterneurotransmitter,
chemical that transmits information across the junction (synapse) that separates one nerve cell (neuron) from another nerve cell or a muscle. Neurotransmitters are stored in the nerve cell's bulbous end (axon).
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. It is particularly important in the stimulation of muscle tissue. The transmission of an impulse to the end of the nerve causes it to release neurotransmitter molecules onto the surface of the next cell, stimulating it. After such release, the acetylcholine is quickly broken into acetate and choline, which pass back to the first cell to be recycled into acetylcholine again. The poison curarecurare
, any of a variety of substances originally used as arrow poisons by Native South Americans in hunting and in warfare. The main active substance of curare, tubocurarine, is an alkaloid extracted from Chondodendron tomentosum, Strychnos toxifera,
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 acts by blocking the transmission of acetylcholine. Some nerve gases operate by preventing the breakdown of acetylcholine causing continual stimulation of the receptor cells, which leads to intense spasms of the muscles, including the heart. Acetylcholine is often abbreviated as Ach. See nervous systemnervous system,
network of specialized tissue that controls actions and reactions of the body and its adjustment to the environment. Virtually all members of the animal kingdom have at least a rudimentary nervous system.
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A naturally occurring quaternary ammonium cation ester, with the formula CH3(O)COC2H4N(CH)3+, that plays a prominent role in nervous system function. The great importance of acetylcholine derives from its role as a neurotransmitter for cholinergic neurons, which innervate many tissues, including smooth muscle and skeletal muscle, the heart, ganglia, and glands. The effect of stimulating a cholinergic nerve, for example, the contraction of skeletal muscle or the slowing of the heartbeat, results from the release of acetylcholine from the nerve endings.

Acetylcholine is synthesized at axon endings from acetyl coenzyme A and choline by the enzyme choline acetyltransferase, and is stored at each ending in hundreds of thousands of membrane-enclosed synaptic vesicles. When a nerve impulse reaches an axon ending, voltage-gated calcium channels in the axonal membrane open and calcium, which is extremely low inside the cell, enters the nerve ending. The increase in calcium-ion concentration causes hundreds of synaptic vesicles to fuse with the cell membrane and expel acetylcholine into the synaptic cleft (exocytosis). The acetylcholine released at a neuromuscular junction binds reversibly to acetylcholine receptors in the muscle endplate membrane, a postsynaptic membrane that is separated from the nerve ending by a very short distance. The receptor is a cation channel which opens when two acetylcholine molecules are bound, allowing a sodium current to enter the muscle cell and depolarize the membrane. The resulting impulse indirectly causes the muscle to contract.

Acetylcholine must be rapidly removed from a synapse in order to restore it to its resting state. This is accomplished in part by diffusion but mainly by the enzyme acetylcholinesterase, which hydrolyzes acetylcholine.

Acetylcholinesterase is a very fast enzyme: one enzyme molecule can hydrolyze 10,000 molecules of acetylcholine in 1 s. Any substance that efficiently inhibits acetylcholinesterase will be extremely toxic.



an acetic acid ester of choline: CH3COOCH2CH2N(CH3)3OH. Colorless crystals, readily soluble in water, alcohol, and chloroform; insoluble in ether. Its molecular weight is 163.2.

Acetylcholine is a biologically active substance widely distributed in nature. It is found in the tissues of organisms in small quantities (fractions of a microgram) in the form of an inactive compound with proteins and lipides; in certain pathological states, the acetylcholine content of the blood is increased. Acetylcholine in its active state is formed in the organism from acetic acid and choline under the action of the enzyme cholinacetylase; it is readily decomposed by enzymes of the cholinesterase group. Acetylcholine belongs to the group of mediators—transmitters of nerve stimuli in the peripheral and central nervous systems. It is secreted by the endings of the autonomic and motor nerve fibers and causes a specific reaction on the part of the innervating organ to stimulate a given nerve. Tiny sacs (vesicles) containing acetylcholine have been discovered in the presynaptic nerve endings. When a nerve is stimulated, acetylcholine enters the synaptic gap from these sacs; this effects transmission of the nerve impulse. When acetylcholine penetrates organs and tissues, it may cause effects characteristic of the excitation of the parasympathetic elements of the autonomic nervous system (lowering of blood pressure, slowing of heartbeat, increased peristalsis of stomach and intestines, pupilar contraction, and so on). The action of certain cholinesterase inhibitors (carbamates, organophosphorous insecticides, and certain poisonous substances) leads to the accumulation of excessive quantities of acetylcholine in the organism, which at first causes acceleration of nerve-impulse transmission (excitation) and later leads to termination of transmission—that is, the blocking of impulses (paralysis). Determination of acetylcholine is made principally by means of biological indicators—contraction of the spinal muscle in leeches and of the straight muscle of the abdomen in frogs, decrease in blood pressure in cats, and so on.


Fiziologicheskaia rol’ atsetilkholina i izyskanie novykh lekarstvennykh veshchestv Leningrad, 1957.
Al’pern, D. E. Kholinergicheskie protsessy ν patologii. Moscow, 1963.



C7H17O3N A compound released from certain autonomic nerve endings which acts in the transmission of nerve impulses to excitable membranes.
References in periodicals archive ?
Basic characteristics of the antimuscarinic drugs Darifenacin 507.5 Low M3 Fesoterodine 527.6 Low Non-selective Oxybutynin 393.9 High Non-selective Propiverine 403.9 (*) Limited data Non-selective Solifenacin 480.5 Moderate Predominantly M3 Tolterodine 475.6 Moderate Non-selective Trospium 427.9 Low Non-selective BBB: Blood-brain barrier, (*) Value expressed in g/moL Table 2.
Treatment-naive patients taking mirabegron demonstrated statistically significantly greater persistence compared with those taking antimuscarinic drugs (Table 3, Fig.
A lower incidence of anticholinergic adverse events with mirabegron seen in clinical trials may explain the improved persistence and adherence rates compared with antimuscarinic drugs. However, the persistence rate of 31.7% with mirabegron at 12 months in this study still means that about two-thirds of patients discontinued treatment, with a similar gradient of decline in persistence over time to that seen with antimuscarinics.
Postoperatively, 1 patient (3.1%) had de novo urgency, but UDS were normal and she was treated with an antimuscarinic drug. Vaginal erosion was not documented in any of the patients.
The newer antimuscarinic drugs: bladder control with less dry mouth.
Although selection of the second antimuscarinic drug for combination was at the physician's discretion, a drug that had not been used as monotherapy was preferred as the second antimuscarinic drug.
In clinical practice, patients are considered to have refractory UUI if they have failed at least 2 adequate treatments of antimuscarinic drugs. OnabotuliniumtoxinA (BoNT-A) (off-label), neuromodulation and surgical interventions, such as augmentation cystoplasty, are all acceptable options for a small percentage of patients who do not respond to conservative and drug therapies depending on availability of resources.
For UUI or MUI, antimuscarinic drugs can be prescribed with varying success rates (level of evidence 2, grade B).[sup.30] When starting therapy, important factors, including polypharmacy, pharmacokinetics, adverse drug reactions, drug-drug interactions and drug-disease interactions, must be considered.[sup.14,15] Moreover, dose titration regimen and evaluation of the balance between clinical benefits and side effects should be considered.
Antimuscarinic drugs are first-line treatment for the overactive bladder syndrome (OAB).
Research has suggested that antimuscarinic drugs exert their therapeutic benefit through effects on afferent activity during the filling phase and that there is no proof that, at approved doses, they reduce the ability to empty the bladder.[sup.14] There is a theoretical potential of these agents to have an effect on voiding contraction, but the concentration of antimuscarinic required to achieve this effect would be limited by the potential for side effects.
Table 1.: Advantages and disadvantages of antimuscarinic drugs for overactive bladder [Table omitted]
The evidence for adding estrogen in combination with an antimuscarinic drug is equivocal.