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By directly stimulating cholinergic receptors, cholinergic agonists mimic the action of the neurotransmitter acetylcholine.
They include such drugs as:
The action and metabolism of cholinergic agonists vary widely and depend on the affinity of the individual drug for muscarinic or nicotinic receptors.
Cholinergic agonists rarely are administered by I.M. or I.V. injec-tion because they’re almost immediately broken down by cholin-esterases in the interstitial spaces between tissues and inside the blood vessels. Moreover, they begin to work rapidly and can cause a cholinergic crisis (a drug overdose resulting in extreme muscle weakness and possibly paralysis of the muscles used in respira-tion).
Cholinergic agonists are usually administered:
· topically, with eye drops
· by subcutaneous (subQ) injection.
SubQ injections begin to work more rapidly than oral doses.
All cholinergic agonists are metabolized by cholinesterases:
· at the muscarinic and nicotinic receptor sites
· in the plasma (the liquid portion of the blood)
· in the liver.
All drugs in this class are excreted by the kidneys.
Cholinergic agonists work by mimicking the action of acetylcho-line on the neurons in certain organs of the body called target or-gans. When they combine with receptors on the cell membranesof target organs, they stimulate the muscle and produce:
· bradycardia (a slow heart rate)
· dilation of blood vessels
· constriction of the bronchioles
· increased activity of the GI tract
· increased tone and contraction of the bladder muscles
· constriction of the pupils.
Cholinergic agonists are used to:
§ treat atonic (weak) bladder conditions and postoperative and postpartum urine retention
§ treat GI disorders, such as postoperative abdominal distention and GI atony
§ reduce eye pressure in patients with glaucoma and during eye surgery
§ treat salivary gland hypofunction caused by radiation therapy or Sjögren’s syndrome.
Cholinergic agonists have specific interactions with other drugs.
Examples include the following:
· Other cholinergic drugs, particularly anticholinesterase drugs (such as ambenonium, edrophonium, neostigmine, physostigmine, and pyridostigmine), boost the effects of cholinergic agonists and increase the risk of toxicity.
· Cholinergic blocking drugs (such as atropine, belladonna, ho-matropine, methantheline, methscopolamine, propantheline, and scopolamine) reduce the effects of cholinergic drugs.
· Quinidine also reduces the effectiveness of cholinergic agonists. (See Adverse reactions to cholinergic agonists.)
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