Cholinergic Agonists

High-yield Verified · Oct 2026

Prototype: bethanechol

Cholinergic Agonists are a class of medications used for urinary retention / neurogenic bladder and postoperative ileus.

Medical view → mechanisms, drug comparisons and Step 1 pharmacology

Direct and indirect agents that boost acetylcholine effect — the parasympathetic accelerator.

How it works in the body

The system involved, what goes wrong, and how the drug and body interact.

01 The “rest-and-digest” system and acetylcholine

The parasympathetic (“rest-and-digest”) branch of the autonomic nervous system runs the body’s calm, housekeeping functions — and it signals through one neurotransmitter: acetylcholine (ACh) acting on muscarinic receptors. When ACh fires, the body slows the heart, constricts pupils, and stimulates the gut, bladder, and glands (saliva, tears, sweat).

Cholinergic agonists boost that ACh signal. They’re used where a body function is under-active: a hypotonic bladder that won’t empty (urinary retention), dry mouth/eyes, glaucoma (contracting the ciliary muscle opens the eye’s drainage meshwork), and the muscle weakness of myasthenia gravis. Two drugs turn the same pharmacology to other ends: inhaled methacholine deliberately narrows the airways to test for airway hyperreactivity, and IV physostigmine reverses anticholinergic poisoning.

02 Two ways to raise acetylcholine — direct vs indirect

Direct agonists (bethanechol, pilocarpine, methacholine, carbachol, cevimeline) are ACh-like molecules that bind muscarinic receptors themselves — bethanechol targets the bladder/GI tract (urinary retention, ileus), pilocarpine the eye and salivary glands, cevimeline the salivary glands (dry mouth in Sjögren syndrome), carbachol the eye (placed inside it to constrict the pupil during surgery), and inhaled methacholine the airways, where it is used only to provoke bronchoconstriction in a diagnostic challenge test. Indirect agonists work by blocking the enzyme acetylcholinesterase, which normally breaks ACh down — so ACh piles up and its effect is amplified everywhere.

The indirect cholinesterase inhibitors — usually pyridostigmine (neostigmine is available but used less often) — are first-line symptomatic therapy for myasthenia gravis (more ACh at the neuromuscular junction restores strength) and are used to reverse non-depolarizing neuromuscular blockers after surgery. (Their CNS-penetrating cousins — donepezil, rivastigmine — are used in Alzheimer disease.) Physostigmine acts in the brain as well as the body: given IV, it reverses the central effects (delirium) of severe anticholinergic poisoning. It is not an FDA-approved drug — the US physostigmine injection’s labeling carries the FDA notice that the drug has not been found safe and effective, and Anticholium, a German product that the FDA has allowed to be imported temporarily to relieve a US shortage, is not FDA-approved either. Most of these drugs inhibit the enzyme reversibly; echothiophate eye drops are a long-acting, irreversible inhibitor — grouped with the organophosphate insecticides and nerve agents — used to lower raised eye pressure and in accommodative esotropia.

Loading diagram…

Direct agonists mimic ACh; indirect agonists block its breakdown — both raise cholinergic effect.

03 Too much of a good thing — cholinergic crisis (SLUDGE)

Push cholinergic effect too far and every parasympathetic action fires at once — a cholinergic crisis. The picture is captured by SLUDGE: Salivation, Lacrimation, Urination, Diarrhea, GI cramping, Emesis — plus the three Bs commonly added to it — bradycardia, bronchorrhea and bronchospasm, the signs that can kill and the ones atropine reverses — and miosis (tiny pupils). With a cholinesterase inhibitor, the crisis also brings increasing muscle weakness, which can spread to the breathing muscles and be fatal. The same syndrome is what organophosphate (pesticide/nerve-agent) poisoning produces.

The antidote is atropine (an anticholinergic that blocks the muscarinic receptors) — the mirror-image drug in this system. For a myasthenia patient, distinguishing cholinergic crisis (too much drug) from a myasthenic crisis (too little) is critical because the treatments are opposite.

Loading diagram…

Overdose → cholinergic crisis: SLUDGE plus the three Bs (bradycardia, bronchorrhea, bronchospasm). Antidote: atropine.

Drug names

Generic Brand

bethanechol —

pilocarpine Salagen

methacholine Provocholine

carbachol Miostat

cevimeline Evoxac

neostigmine —

pyridostigmine Mestinon

physostigmine Anticholium

echothiophate Phospholine Iodide

* Anticholium (physostigmine): Not FDA-approved. A German product imported under a temporary importation license to address a US shortage.

Indications

Urinary retention / neurogenic bladder & postoperative ileus (bethanechol, neostigmine)
Myasthenia gravis (pyridostigmine, neostigmine); reversal of non-depolarizing NMB (neostigmine)
Glaucoma and dry mouth/eyes (pilocarpine)
Cevimeline for dry mouth in Sjögren syndrome
Carbachol placed inside the eye for miosis during surgery and to reduce the pressure rise in the first 24 hours after cataract surgery; carbachol with brimonidine (Yuvezzi eye drops) for presbyopia
Methacholine (inhaled) for the methacholine challenge test — diagnosing airway hyperreactivity in people without clinically apparent asthma
Physostigmine, given IV and not FDA-approved, to reverse the central nervous system effects of anticholinergic poisoning
Echothiophate eye drops for elevated intraocular pressure and accommodative esotropia

Mechanism of action

Direct agonists (bethanechol, pilocarpine, methacholine, carbachol, cevimeline) stimulate muscarinic receptors; indirect agonists (neostigmine, pyridostigmine, physostigmine; echothiophate irreversibly) inhibit acetylcholinesterase, increasing synaptic acetylcholine at muscarinic and neuromuscular-junction nicotinic receptors.

In plain terms

They ramp up the “rest-and-digest” signal — either by imitating acetylcholine or by stopping its breakdown.

Therapeutic effects — what you'll see working

Success depends on the use: a bladder that empties, improved strength in myasthenia, reversal of paralysis after surgery, relief of dry mouth, or — after physostigmine — the return of alertness and orientation in anticholinergic poisoning. The dose is titrated carefully because the margin to cholinergic excess is real.

Bladder/GI stimulation Restored muscle strength (myasthenia) NMB reversal / glaucoma / secretions Airway testing and antidote use

Bladder/GI stimulation: Bethanechol increases detrusor and GI tone, helping a hypotonic bladder empty and relieving non-obstructive urinary retention or ileus.
Restored muscle strength (myasthenia): More ACh at the neuromuscular junction (pyridostigmine) improves the weakness of myasthenia gravis.
NMB reversal / glaucoma / secretions: Neostigmine reverses non-depolarizing paralytics; pilocarpine lowers eye pressure and stimulates saliva, as cevimeline does; echothiophate lowers eye pressure, and intraocular carbachol constricts the pupil.
Airway testing and antidote use: Inhaled methacholine narrows hyperreactive airways at lower doses than normal ones — the basis of the challenge test; IV physostigmine reverses the delirium of anticholinergic poisoning.

Adverse effects

Every adverse effect is the parasympathetic system doing its job too much — the SLUDGE picture, plus bradycardia and bronchospasm.

Common

Salivation, sweating, lacrimation, nausea, abdominal cramping, diarrhea, urinary urgency, blurred vision/miosis.

These are ordinary muscarinic effects and often dose-limiting — the same SLUDGE letters in mild form.

Serious — cholinergic crisis Report immediately

Bradycardia, hypotension, bronchospasm/bronchorrhea, full SLUDGE and, with cholinesterase inhibitors, increasing muscle weakness — a cholinergic crisis. Treated with atropine.

Excess effect can cause dangerous bradycardia, bronchoconstriction with copious secretions, and respiratory compromise. With a cholinesterase inhibitor, weakness that reaches the breathing muscles can be fatal: the drug is stopped promptly and atropine is given — atropine counters the muscarinic effects, not the weakness, so breathing support may be needed. In myasthenia, distinguish this from a myasthenic (undertreatment) crisis.

■ Boxed warning · methacholine Report immediately

Severe bronchoconstriction can follow inhaled methacholine, even at the lowest dose of the challenge test.

Methacholine is contraindicated when baseline lung function is low (FEV1 below 60% of predicted, or below 1.5 L in adults) and not recommended with clinically apparent asthma or wheezing. Emergency equipment and medication must be immediately available, and severe bronchoconstriction is reversed at once with a rapid-acting inhaled β-agonist. If baseline spirometry is skipped or inaccurate, falls in FEV1 can be missed and unnecessary higher doses given.

Serious — physostigmine given too fast Report immediately

Bradycardia, excess salivation with breathing difficulty, and seizures when the IV injection is too rapid; an overdose can cause a cholinergic crisis.

Physostigmine is injected slowly. Excessive salivation, vomiting, urination or defecation means the drug is stopped, and atropine — its antidote — is kept at hand. In tricyclic antidepressant poisoning cardiac arrest is possible, so physostigmine is considered there only with continuous ECG monitoring.

Eye drugs — carbachol, echothiophate Hold & notify

Blurred or dim vision, eye pain, stinging and redness; rarely retinal detachment. With echothiophate, also iris cysts (more often in children) and lens opacities.

Miotics can cause accommodative spasm and temporarily dim vision, so night driving and other tasks in poor light need caution. Sudden flashes of light, floaters or vision loss need immediate care (possible retinal tear or detachment). Echothiophate drops also lower plasma and red-cell cholinesterase after a few weeks of use, which matters if succinylcholine is planned for anesthesia.

Antidote

Atropine

Blocks muscarinic receptors — reverses cholinergic excess (SLUDGE) and the accompanying bradycardia in a cholinergic crisis. In organophosphate poisoning, atropine is given with pralidoxime, which reactivates cholinesterase and treats both muscarinic and nicotinic effects (it works only early, before the enzyme “ages”).

Interactions

Bethanechol with ganglion-blocking drugs drug

A critical fall in blood pressure may occur — special care is needed; severe abdominal symptoms usually come first.

Oral pilocarpine with β-blockers drug

Possible conduction disturbances — caution.

Oral pilocarpine with other cholinergic or with antimuscarinic drugs drug

Additive effects with parasympathomimetics; pilocarpine may work against the anticholinergic effect of drugs that rely on it (e.g. atropine, inhaled ipratropium).

Neostigmine with succinylcholine (depolarizing blockers) drug

Not used to reverse a depolarizing block — it may prolong the phase I block.

Neostigmine with neomycin, streptomycin or kanamycin drug

These antibiotics have their own nondepolarizing blocking action, so the neostigmine dose needed to reverse the block may need adjusting.

Neostigmine with drugs that alter liver enzymes drug

Neostigmine is metabolized by hepatic microsomal enzymes, so its level may rise with enzyme inhibitors or fall with inducers — monitor for longer.

Pyridostigmine with succinylcholine or nondepolarizing blockers (e.g. pancuronium) drug

Pyridostigmine taken before surgery can enhance a depolarizing (succinylcholine) block, so particular caution is needed, and the dose of a nondepolarizing blocker may need to be increased.

Pyridostigmine with aminoglycosides (and some other antibiotics), antiarrhythmics such as quinidine, or local and some general anesthetics drug

These interfere with neuromuscular transmission and are used cautiously, if at all: high-dose antibiotics can intensify or produce neuromuscular block, and quinidine has been followed by recurrent paralysis after a block was reversed.

Pyridostigmine with opioids drug

The bradycardia opioids cause may add to pyridostigmine’s bradycardia.

Pyridostigmine with mefloquine drug

May have additive effects on the gut — most often loose bowels — and on the atrial rate.

Pyridostigmine with anticholinesterase eye drops for glaucoma (e.g. echothiophate) drug

An additive effect that may cause or worsen problems with night vision (see also the echothiophate row below).

Pyridostigmine with dexpanthenol (drugs converted to pantothenic acid) drug

May add to pyridostigmine’s effect by increasing acetylcholine production.

Pyridostigmine injection (reversal of neuromuscular blockade) with 4-aminopyridine drug

Reported to delay the onset of action of injected pyridostigmine.

Methacholine with β-blockers drug

May impair reversal of methacholine-induced bronchoconstriction.

Methacholine with β-agonists, inhaled anticholinergics, or theophylline drug

They blunt the airway response to methacholine, so they are held before the challenge test for the times the label lists; regular corticosteroids or inhaled cromoglycate may also lessen the response but can be continued.

Physostigmine with other cholinesterase inhibitors (e.g. dementia drugs) drug

Potentiated cholinergic effects — caution.

Physostigmine with succinylcholine (depolarizing blockers) drug

Contraindicated — physostigmine can deepen the depolarizing block and worsen paralysis.

Cevimeline with β-blockers drug

Possible conduction disturbances — caution.

Cevimeline with CYP2D6 or CYP3A4 inhibitors drug

They slow cevimeline’s metabolism; people with low CYP2D6 activity may be at higher risk of adverse events.

Cevimeline with other cholinergic or with antimuscarinic drugs drug

Additive effects with parasympathomimetics; cevimeline may interfere with the intended effect of antimuscarinics.

Echothiophate with succinylcholine, systemic cholinesterase inhibitors, or organophosphate/carbamate insecticides drug

Echothiophate potentiates them — succinylcholine only with great caution, if at all (possible respiratory or cardiovascular collapse), and additive systemic effects with the others.

Contraindications

The labeled contraindications are places where added parasympathetic tone is dangerous — asthma (bethanechol, oral pilocarpine, cevimeline, physostigmine), an obstructed GI or urinary outlet (bethanechol, neostigmine, pyridostigmine and physostigmine), and, for bethanechol, the slow heart, low blood pressure, peptic ulcer, hyperthyroidism, coronary disease, epilepsy, parkinsonism, and a recently operated or inflamed bladder or bowel. Oral pilocarpine and cevimeline are also contraindicated wherever a small pupil is unwanted (acute iritis, narrow-angle glaucoma). Methacholine is contraindicated when baseline lung function is low; physostigmine with diabetes, gangrene, cardiovascular disease, a vagotonic state or a depolarizing neuromuscular blocker; and echothiophate with active uveal inflammation or most angle-closure glaucoma without iridectomy.

Asthma (bethanechol: latent or active asthma; oral pilocarpine and cevimeline: uncontrolled asthma; physostigmine: asthma)

Labeled contraindication — cholinergic stimulation causes bronchospasm and increased secretions.

COPD, or asthma with neostigmine, pyridostigmine or echothiophate use caution

Cholinergic stimulation causes bronchospasm and increased secretions — a labeled caution rather than a listed contraindication for these products.

Mechanical GI or urinary obstruction (bethanechol, neostigmine, pyridostigmine, physostigmine)

Labeled contraindication — stimulating contraction against a blockage risks perforation (bethanechol is for nonobstructive retention).

Bethanechol with hyperthyroidism, peptic ulcer, pronounced bradycardia or hypotension, or coronary artery disease

Labeled contraindications — added vagal tone slows the heart further, increases acid, and can trigger arrhythmia in hyperthyroidism.

Bethanechol with epilepsy, parkinsonism, vasomotor instability, marked vagotonia, or hypersensitivity to the drug

Labeled contraindications for bethanechol.

Bethanechol after recent bladder surgery or bowel resection/anastomosis, or with peritonitis, acute GI inflammation, spastic GI disturbances, bladder-neck obstruction, or a weakened bladder or bowel wall

Labeled contraindications — stronger bladder and gut contractions could harm a healing, inflamed, or weakened wall.

Neostigmine or pyridostigmine with bradycardia, cardiac conduction disease, or peptic ulcer disease use caution

Added vagal tone slows the heart further and increases acid — a caution rather than a listed contraindication for these drugs.

Oral pilocarpine (Salagen) or cevimeline with acute iritis, narrow-angle glaucoma, or hypersensitivity to the drug

Labeled contraindications — the drug constricts the pupil, which is harmful in these eye conditions.

Methacholine with baseline FEV1 below 60% of predicted (or below 1.5 L in adults), or hypersensitivity to methacholine or other parasympathomimetic drugs

Labeled contraindications (low lung function is also in the boxed warning) — the challenge test can cause severe bronchoconstriction.

Methacholine challenge with clinically apparent asthma or wheezing, uncontrolled hypertension, aortic aneurysm, a history of myocardial infarction or stroke, or pregnancy use caution

The label does not recommend the test in these settings (in pregnancy because of possible fetal hypoxia); epilepsy, vagotonia, peptic ulcer, thyroid disease or urinary obstruction call for a benefit–risk judgment first.

Physostigmine with asthma, gangrene, diabetes, cardiovascular or coronary disease, mechanical bowel or urinary obstruction, a vagotonic state, myotonic dystrophy, or closed traumatic brain injury

Labeled contraindications for physostigmine.

Physostigmine with succinylcholine or another depolarizing neuromuscular blocker, with choline esters, or in poisoning with irreversible cholinesterase inhibitors (organophosphates) or barbiturates

Labeled contraindications — physostigmine can deepen a depolarizing block and worsen paralysis, and other cholinesterase inhibitors add to its cholinergic effects.

Echothiophate with active uveal inflammation, most angle-closure glaucoma without an iridectomy, or hypersensitivity

Labeled contraindications — the drug can increase angle block and can activate latent iritis or uveitis.

Echothiophate with marked vagotonia, asthma, spastic GI disturbances, peptic ulcer, pronounced bradycardia and hypotension, recent myocardial infarction, epilepsy, parkinsonism, or a prior retinal detachment use caution

Label precautions — to be used with caution, if at all, where vagotonic effects could cause harm.

Intraocular carbachol (Miostat) with acute heart failure, asthma, peptic ulcer, hyperthyroidism, GI spasm, urinary tract obstruction, or Parkinson disease use caution

Label cautions; its only listed contraindication is hypersensitivity (the vial stopper also contains natural rubber latex).

Cevimeline with cardiovascular disease (angina or prior myocardial infarction), controlled asthma or COPD, or kidney or gallbladder stones use caution

Label warnings — it can alter heart rate and conduction, raise airway resistance and secretions, and contract biliary and ureteral smooth muscle (cholecystitis, biliary obstruction, renal colic).

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Administration & monitoring

Give bethanechol on an empty stomach; keep the patient near a bathroom and watch for SLUDGE effects.

Why: Food causes nausea/vomiting, and the drug rapidly stimulates the bladder and gut.

Keep atropine available as the antidote; monitor heart rate and respiratory status.

Why: Cholinergic excess causes bradycardia and bronchospasm; atropine reverses it.

For neostigmine (NMB reversal), give atropine or glycopyrrolate first; in cardiac disease, arrhythmias or a recent coronary occlusion, monitor BP and ECG continuously.

Why: The anticholinergic lessens neostigmine’s bradycardia, and these cardiac patients are especially sensitive to its effects on heart rate and blood pressure.

In myasthenia, give pyridostigmine on time and distinguish cholinergic vs myasthenic crisis.

Why: Timing maintains strength; the two crises look similar but have opposite treatments.

If atropine is used to blunt pyridostigmine’s GI side effects, watch closely for rising weakness.

Why: Atropine can mask the warning signs of overdose and let a cholinergic crisis develop unnoticed.

For a methacholine challenge, confirm that baseline spirometry has been done and have emergency equipment and a rapid-acting inhaled β-agonist ready; the β-agonist is also given after the test.

Why: Severe bronchoconstriction can occur even at the lowest dose; the post-test β-agonist speeds the return of lung function to baseline.

Before the test, check that bronchodilators (β-agonists, inhaled anticholinergics, theophylline) were held for the times the label lists, and note any β-blocker; staff avoid inhaling the powder or aerosol.

Why: Bronchodilators blunt the airway response to methacholine, β-blockers may impair reversal of the bronchoconstriction, and the aerosol can narrow the airways of the people giving the test.

Give IV physostigmine slowly, with ECG monitoring and atropine at the bedside; stop it if salivation, vomiting, urination or defecation become excessive.

Why: Rapid injection causes bradycardia, hypersalivation with breathing difficulty, and seizures; atropine is its antidote, and cardiac arrest is possible in tricyclic antidepressant poisoning.

Judge physostigmine’s effect by the return of alertness and orientation (name, address, date), and keep watching — the dose may need repeating if the symptoms come back.

Why: Recovery of mental function is the label’s measure of adequate dosing, and physostigmine is short-acting, so the anticholinergic signs can recur.

Make sure the anesthesia team knows a patient uses echothiophate eye drops before succinylcholine is considered.

Why: The drops lower plasma cholinesterase; succinylcholine is then given only with great caution, if at all, because of possible respiratory or cardiovascular collapse.

Before intraocular carbachol (Miostat) is used, check for a latex allergy.

Why: The vial stopper contains natural rubber latex, which may cause severe allergic reactions.

Review the medication list before cevimeline: β-blockers and drugs that inhibit CYP2D6 or CYP3A4 need caution.

Why: β-blockers add a risk of conduction disturbances; CYP2D6 and CYP3A4 inhibitors slow cevimeline’s metabolism, and people with low CYP2D6 activity may be at higher risk of adverse events.

Patient teaching

Report excess salivation/sweating, diarrhea, wheezing, or a slow heart rate.

Why: These signal cholinergic excess before it becomes a crisis.

With bethanechol, get up slowly from lying or sitting; report dizziness, lightheadedness, or fainting.

Why: Muscarinic vasodilation can lower blood pressure on standing (postural hypotension).

Before pilocarpine eye drops (or carbachol–brimonidine, Yuvezzi) are started, the patient needs a retinal (fundus) exam.

Why: Rare retinal detachment has occurred with miotics, especially with existing retinal disease.

With cevimeline, take care driving at night, and drink extra water if sweating heavily.

Why: It can cause visual disturbances, especially at night, and excessive sweating can lead to dehydration.

After echothiophate drops, press on the inner corner of the eye for a minute or two and wash the hands; stop and report salivation, urinary incontinence, diarrhea, heavy sweating, muscle weakness, or breathing difficulty.

Why: Pressure limits drainage into the nose and throat and washing prevents skin absorption; these systemic cholinergic signs mean the drug must be stopped for a time.

Patients using echothiophate who are exposed to organophosphate or carbamate insecticides should protect themselves (respiratory masks, frequent washing and clothing changes).

Why: Pesticide absorbed through the lungs or skin adds to the drug’s systemic effects.

With Yuvezzi (carbachol–brimonidine) drops, take care driving at night or in poor light, and get immediate care for sudden flashes of light, floaters, or vision loss.

Why: Miotics can blur and dim vision, and rare retinal tears and detachments have occurred with them.

Common questions

What are Cholinergic Agonists used for?

Cholinergic Agonists are used for urinary retention / neurogenic bladder and postoperative ileus, myasthenia gravis, and glaucoma and dry mouth/eyes. Cevimeline for dry mouth in Sjögren syndrome. Carbachol placed inside the eye for miosis during surgery and to reduce the pressure rise in the first 24 hours after cataract surgery. Methacholine for the methacholine challenge test. Physostigmine, given IV and not FDA-approved, to reverse the central nervous system effects of anticholinergic poisoning. Echothiophate eye drops for elevated intraocular pressure and accommodative esotropia.

How do Cholinergic Agonists work?

They ramp up the “rest-and-digest” signal — either by imitating acetylcholine or by stopping its breakdown.

What are the serious side effects of Cholinergic Agonists?

Watch for bradycardia, hypotension, bronchospasm/bronchorrhea, full SLUDGE and, with cholinesterase inhibitors, increasing muscle weakness — a cholinergic crisis. Treated with atropine; severe bronchoconstriction can follow inhaled methacholine, even at the lowest dose of the challenge test; (with physostigmine) bradycardia, excess salivation with breathing difficulty, and seizures when the IV injection is too rapid; an overdose can cause a cholinergic crisis.

What is the antidote for Cholinergic Agonists toxicity?

The antidote is Atropine. Blocks muscarinic receptors — reverses cholinergic excess (SLUDGE) and the accompanying bradycardia in a cholinergic crisis. In organophosphate poisoning, atropine is given with pralidoxime, which reactivates cholinesterase and treats both muscarinic and nicotinic effects (it works only early, before the enzyme “ages”).

Conditions treated

Myasthenia Gravis

Patho · Nervous

The first-line symptomatic therapy — pyridostigmine should initiate most treatment regimens. As an anticholinesterase it raises the level and duration of ACh at the junction so the surviving receptors are stimulated more; onset 15–30 min, duration 3–4 h, so doses are scheduled through the day, given exactly on time and about one hour before meals so peak strength coincides with chewing and swallowing. Extended-release tablets are swallowed whole; a missed dose is never doubled. Its adverse effects are muscarinic excess — cramping, loose stools, sweating, drooling — and overdose is cholinergic crisis. Two exam rules: MuSK patients respond poorly and get side effects at usual doses, and during crisis or ventilation the drug is held or sharply reduced, never added, because it increases airway secretions.

Scleroderma & Sjögren’s

Patho · Immune / Infectious

Dry mouth (both diseases). "Prescription medications like pilocarpine (Salagen) or cevimeline (Evoxac) stimulate salivary flow" (Sjögren’s); in scleroderma, "secretagogues such as pilocarpine or cevimeline can also alleviate dry mouth." NIAMS: they also "stimulate tear production."

Urinary Incontinence

Patho · Renal / Genitourinary

[Overflow] Bethanechol, "a detrusor stimulant," helps a weak detrusor contract.

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Always verify against current prescribing information and your institution's protocols before administering. Not medical advice.