antimuscarinic drugs


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acetylcholine (ACh) 

A neurotransmitter substance with special excitatory properties of all preganglionic autonomic neurons, all parasympathetic postganglionic neurons and a few postganglionic sympathetic neurons. Acetylcholine is synthesized and liberated by the action of the enzyme choline acetyltranferase from the compounds choline and acetyl coenzyme A (acetyl CoA) which occurs in all cholinergic neurons. ACh exists only momentarily after its formation, being hydrolysed by the enzyme acetylcholinesterase which is present in the neurons of cholinergic nerves throughout their entire lengths and at neuromuscular junctions: this process is essential for proper muscle function as otherwise the accumulation of ACh would result in continuous stimulation of the muscles, glands and central nervous system. Alternatively a shortage of ACh has devastating effect (e.g. myasthenia gravis). ACh binds to acetylcholine receptors on skeletal muscle fibres. Sodium enters the muscle fibre membrane, which leads to a depolarization of the membrane and muscle contraction. There are two main types of acetylcholine receptors (cholinergic receptors): muscarinic receptors, which are stimulated by muscarine and ACh, belong to a family of G proteins coupled receptors and are situated in parasympathetically innervated structures (e.g. the iris and ciliary body); and nicotine receptors, which are stimulated by nicotine and ACh, are ligand-gated receptors and are situated in striated muscles (e.g. the extraocular muscles). Cholinergic receptors are found in the sympathetic and parasympathetic nervous systems, in the brain and spinal cord. The action of ACh can be either blocked or stimulated by drugs: Anticholinesterase drugs (e.g. neostigmine) inhibit acetylcholinesterase and prolong the action of acetylcholine whereas antimuscarinic drugs (also referred to as anticholinergics or parasympatholytics) such as atropine, cyclopentolate, homatropine, hyoscine and tropicamide inhibit the action of acetylcholine at muscarinic receptors. Other drugs mimic the action of ACh, they are known as parasympathomimetics (e.g. pilocarpine). See cholinergic; cycloplegia; miotics; mydriatic; neurotransmitter; nicotine; synapse; autonomic nervous system.

mydriatic

1. Causing mydriasis of the pupil. 2. A drug which produces mydriasis. Mydriatics are used to carry out a thorough inspection of the fundus and lens, especially in elderly patients in whom the pupils are usually smaller. However, in older people it must be ascertained that the patient does not have glaucoma. There are two classes of mydriatics: (1) antimuscarinic (parasympatholytic, anticholinergic, atropine-like) drugs which antagonize the action of acetylcholine at muscarinic receptors in the ciliary muscle, such as atropine, cyclopentolate, homatropine, hyoscine (scopolamine) and tropicamide. Antimuscarinic drugs produce cycloplegia as well. (2) sympathomimetic (adrenergic stimulating) drugs which directly or indirectly stimulate the dilator pupillae muscle which is innervated by the sympathetic division of the autonomic nervous system. These include cocaine, ephedrine hydrochloride, adrenaline (epinephrine), naphazoline and phenylephrine hydrochloride. See adrenergic receptors; cholinergic; cycloplegia; miotics; dilator pupillae muscle; mydriasis; pupil light reflex; sympathomimetic.

antimuscarinic drugs

see muscarinic blocking agents.
References in periodicals archive ?
DR BRUNTON: Although antimuscarinic drug therapy has been shown to improve the symptoms of OAB, persistence is poor, with patients adhering to their prescribed treatment regimens for approximately 3 months on average.
Since 87% of our population received oxybutynin as their index therapy, we can assume that most children were exposed exclusively to oxybutynin in accordance to the fact that it is the only antimuscarinic drug currently approved for the pediatric population.
Regional differences in motor responsiveness to antimuscarinic drugs in rabbit isolated small and large intestine.
Audit of three antimuscarinic drugs for managing retained secretions.
We report our early experience with mirabegron in Canada, using retrospective prescription claims data to compare persistence and adherence versus antimuscarinic drugs over 12 months.
Antimuscarinic drugs relieve detrusor overactivity by blocking M2 and/or M3 receptors in the bladder wall (Andersson, 2011).
Antimuscarinic drugs such as solifenacin (Vesicare) and tolterodine (Detrol), traditionally used for overactive bladder, have been shown to ease urinary symptoms related to BPH.
For these patients with pure SUI, additional treatment, such as antimuscarinic drugs, may be needed after the surgery.
A systematic review and meta-analysis of randomized controlled trials with antimuscarinic drugs for overactive bladder.
In clinical practice, patients are considered to have refractory UUI if they have failed at least 2 adequate treatments of antimuscarinic drugs.