How autonomic drugs are tested on Step 1
Know each receptor's G protein and its main effect.
Cholinergic drugs
Direct agonists act on receptors; cholinesterase inhibitors raise acetylcholine.
| Drug | Mechanism | Use |
|---|---|---|
| Bethanechol | Muscarinic agonist | Postoperative urinary retention and ileus |
| Pilocarpine | Muscarinic agonist | Glaucoma; dry mouth (Sjögren syndrome) |
| Methacholine | Muscarinic agonist | Bronchial challenge test for asthma |
| Neostigmine, pyridostigmine | Cholinesterase inhibitor; no CNS entry | Myasthenia gravis; reversal of neuromuscular blockade |
| Physostigmine | Cholinesterase inhibitor; enters CNS | Anticholinergic toxicity |
| Donepezil, rivastigmine, galantamine | Central cholinesterase inhibitors | Alzheimer disease |
| Atropine | Muscarinic antagonist | Bradycardia, organophosphate poisoning |
| Ipratropium, tiotropium | Inhaled muscarinic antagonists | COPD |
| Oxybutynin, tolterodine | Bladder muscarinic antagonists | Urge incontinence |
| Scopolamine; benztropine | Muscarinic antagonists | Motion sickness; drug-induced parkinsonism |
Glycopyrrolate does not cross the blood-brain barrier and is used to reduce secretions.
Adrenergic drugs
Predict heart rate and blood pressure from the receptors each drug hits.
| Drug | Receptors | Key use or feature |
|---|---|---|
| Epinephrine | α1, α2, β1, β2 | Anaphylaxis, cardiac arrest; β effects dominate at low doses |
| Norepinephrine | α1 > β1 | Septic shock; can cause reflex bradycardia |
| Phenylephrine | α1 | Hypotension, nasal decongestion; reflex bradycardia |
| Dobutamine | β1 > β2 | Cardiogenic shock, heart failure, stress testing |
| Dopamine | D1 → β1 → α1 as dose rises | Shock with bradycardia |
| Albuterol; salmeterol | β2 | Asthma rescue; long-acting control |
| Clonidine; methyldopa | Central α2 agonists | Hypertension (rebound if stopped); methyldopa in pregnancy |
| Cocaine; amphetamine | Block reuptake; release norepinephrine | Sympathomimetic toxidrome |
| Phentolamine | Reversible α blocker | Cocaine or MAOI hypertensive crisis; norepinephrine extravasation |
| Prazosin, doxazosin, tamsulosin | α1 blockers | BPH, hypertension; first-dose orthostatic hypotension |
Indirect sympathomimetics act through released norepinephrine, so their effects fade when stores are depleted.
β blockers
Selectivity and extra properties decide which β blocker fits.
- β1 selective: mostly names A–M (atenolol, betaxolol, bisoprolol, esmolol, metoprolol); safer in asthma and COPD.
- Nonselective: mostly names N–Z (nadolol, pindolol, propranolol, timolol); propranolol also treats essential tremor and migraine prophylaxis.
- α1 and β: carvedilol (heart failure) and labetalol (hypertension in pregnancy, hypertensive emergency).
- Partial agonist activity: pindolol and acebutolol.
- Adverse effects: bradycardia, AV block, bronchospasm, fatigue, erectile dysfunction, and masked symptoms of hypoglycemia. Glucagon treats β blocker overdose.
Worked example
Predict the blood pressure response.
functions Worked example — epinephrine after an α blocker
An experimental animal is given a large dose of an α blocker, then epinephrine. What happens to mean arterial pressure, and why?
- Epinephrine normally raises blood pressure through α1 vasoconstriction plus β1 stimulation of the heart.
- With α receptors blocked, its vasoconstricting effect is lost.
- β2 vasodilation in skeletal muscle beds now dominates and lowers peripheral resistance.
- Mean arterial pressure falls, and heart rate rises from β1 stimulation and reflex.
Answer. Mean arterial pressure falls ("epinephrine reversal") because β2 vasodilation is unopposed.