M1 · Muscarinic
Signal: Gq
Main sites: CNS neurons, enteric ganglia
Predicted effect: Neuronal excitation; supports secretory signaling
This study site merges the attached quick-review spreadsheet and quick-study sheets with the broader FTM2 folder so the autonomic drug map is organized as a teaching resource instead of a raw list. The emphasis is on not missing named drugs, while also making receptor logic easy to follow.
Design goal: dense enough for a professor handout, but still readable at a glance on laptop or tablet.
These receptors are the logic anchors. Once you know location + G-protein/channel + hallmark effect, drug predictions become easier.
Signal: Gq
Main sites: CNS neurons, enteric ganglia
Predicted effect: Neuronal excitation; supports secretory signaling
Signal: Gi
Main sites: Heart: SA and AV node
Predicted effect: Slows SA rate and AV conduction; lowers cAMP; opens K+ channels
Signal: Gq
Main sites: Glands, bronchi, GI tract, bladder, eye sphincter/ciliary muscle, endothelium
Predicted effect: Secretions, bronchoconstriction, gut and bladder contraction, miosis, accommodation; endothelial M3 triggers NO vasodilation
Signal: Ligand-gated cation channel
Main sites: Autonomic ganglia, adrenal medulla
Predicted effect: Fast depolarization of ganglionic neurons and adrenal medulla
Signal: Ligand-gated cation channel
Main sites: Neuromuscular junction
Predicted effect: Skeletal muscle end-plate depolarization and contraction
Signal: Gq
Main sites: Vascular smooth muscle, radial iris, prostate/bladder outlet
Predicted effect: Vasoconstriction, mydriasis, urinary outlet contraction
Signal: Gi
Main sites: Presynaptic terminals, CNS, pancreatic beta cells
Predicted effect: Less NE release, lower central sympathetic output, less insulin secretion
Signal: Gs
Main sites: Heart, juxtaglomerular cells
Predicted effect: Faster and stronger heart activity; increased renin
Signal: Gs
Main sites: Bronchi, vascular smooth muscle, uterus, skeletal muscle
Predicted effect: Bronchodilation, vascular and uterine relaxation, K+ shift into cells
Signal: Gs
Main sites: Adipose tissue
Predicted effect: Lipolysis
Signal: Gs
Main sites: Renal and splanchnic vasculature
Predicted effect: Renal and splanchnic vasodilation
Move from receptor target to mechanism, then to use, then to the trap or adverse effect that exam questions like to test.
| Drug | Target | Use clue | High-yield distinction |
|---|---|---|---|
| ACh (acetylcholine) Cholinergic agonist | M + N Direct agonist; rapid AChE breakdown | Intraocular miosis | IV M3 vasodilation; high dose M2 bradycardia; after atropine, high ACh reveals Nn pressor effect |
| Bethanechol Cholinergic agonist | M Direct muscarinic agonist; AChE resistant | Nonobstructive urinary retention; bladder atony | No useful Nm effect; does not treat myasthenia; avoid mechanical obstruction |
| Methacholine Cholinergic agonist | M Direct muscarinic agonist | Bronchial challenge test | Provokes bronchospasm; not an asthma treatment |
| Pilocarpine Cholinergic agonist | M Tertiary muscarinic agonist | Glaucoma; xerostomia | Miosis, near accommodation, sweating; enters CNS |
| Nicotine Cholinergic agonist | Nn / Nm Nicotinic agonist; high exposure causes block | Smoking cessation; ganglionic stimulation | Affects both autonomic divisions; CNS effects and dependence |
| Edrophonium AChE inhibitor | Indirect M + N Brief reversible AChE inhibition | Historical myasthenia test; reversal | Quaternary, little CNS entry; bradycardia |
| Neostigmine AChE inhibitor | Indirect M + N Reversible carbamate AChE inhibition | Myasthenia; reverses nondepolarizing block | Quaternary; excess ACh causes weakness plus wet symptoms |
| Pyridostigmine AChE inhibitor | Indirect M + N Reversible carbamate AChE inhibition | Myasthenia | Quaternary; longer acting than neostigmine |
| Physostigmine AChE inhibitor | Indirect M + N Tertiary carbamate AChE inhibitor | Selected central antimuscarinic toxicity | Enters CNS, unlike neostigmine |
| Organophosphates (malathion, parathion, chlorothion, sarin) AChE inhibitor | Indirect M + N Prolonged phosphorylated AChE inhibition | Insecticides / nerve-agent recognition | Wet symptoms, miosis, fasciculations, paralysis; atropine blocks M, pralidoxime reactivates AChE before aging |
| Atropine Muscarinic antagonist | M blocker Competitive muscarinic blockade | Bradycardia; secretions; muscarinic poisoning | Dry mouth, hot dry skin, retention, constipation, tachycardia, delirium; mydriasis + cycloplegia; does not block Nm |
| Scopolamine Muscarinic antagonist | M blocker Muscarinic blockade | Motion sickness | Prominent CNS effects |
| Ipratropium Muscarinic antagonist | M blocker Muscarinic blockade | Inhaled bronchodilation | Quaternary agent |
| Tropicamide Muscarinic antagonist | M blocker Muscarinic blockade | Eye dilation | Short ophthalmic action |
| Hexamethonium Ganglion blocker | Nn blocker Ganglionic nicotinic blockade | Historical antihypertensive | Loss of resting tone: vasodilation, orthostasis, tachycardia, constipation, urinary retention, reflex loss |
| Tubocurarine NMJ blocker | Nm blocker Competitive nondepolarizing Nm antagonist | Skeletal muscle relaxation | Reversible with neostigmine plus atropine for muscarinic effects |
| Pancuronium NMJ blocker | Nm blocker Competitive nondepolarizing Nm antagonist | Skeletal muscle relaxation | Longer-acting nondepolarizing blocker |
| Rocuronium NMJ blocker | Nm blocker Competitive nondepolarizing Nm antagonist | Skeletal muscle relaxation | Intermediate duration |
| Vecuronium NMJ blocker | Nm blocker Competitive nondepolarizing Nm antagonist | Skeletal muscle relaxation | Intermediate duration |
| Mivacurium NMJ blocker | Nm blocker Competitive nondepolarizing Nm antagonist | Skeletal muscle relaxation | Shorter duration; uses plasma cholinesterase |
| Succinylcholine Depolarizing NMJ blocker | Nm agonist Sustained depolarization with fasciculations then paralysis | Rapid paralysis / intubation recognition | Hyperkalemia, prolonged apnea, malignant hyperthermia; plasma cholinesterase breakdown; neostigmine worsens phase I block |
| Dantrolene Muscle relaxant adjunct | RyR1 pathway Reduces RyR1 Ca2+ release | Malignant hyperthermia | Acts on skeletal muscle Ca2+ release rather than cholinergic receptor |
| Botulinum toxin Presynaptic blocker | ACh release machinery Cleaves SNAREs to block ACh release | Local spasm; cosmetic/local paralysis | Causes NMJ paralysis without analgesia or unconsciousness |
Predict the direct receptor effect first, then add reflex responses and dose dependence only after that foundation is solid.
| Drug | Receptor logic | Use clue | Trap / exam pearl |
|---|---|---|---|
| Epinephrine Adrenergic agonist | α1, α2, β1, β2 Direct agonist | Anaphylaxis; cardiac arrest | Low dose β2 lowers resistance; high dose α pressor; tachyarrhythmia; α block can reverse pressor response |
| Norepinephrine Adrenergic agonist | α1, α2, β1 Direct agonist; little β2 | Shock | Raises systolic and diastolic BP with reflex bradycardia; extravasation ischemia treated with phentolamine |
| Dopamine Adrenergic agonist | D1 → β1 → α with rising dose Dose-dependent direct agonist | Selected circulatory support | Renal vasodilation does not prove kidney protection; arrhythmias |
| Phenylephrine Adrenergic agonist | α1 Direct agonist | Vasopressor; mydriasis; nasal decongestant example | Reflex bradycardia; mydriasis without direct cycloplegia |
| Clonidine Adrenergic agonist | α2 Central agonist | Lower sympathetic output and BP | Sedation, dry mouth; abrupt stop causes rebound hypertension |
| Isoproterenol Adrenergic agonist | β1, β2 Direct agonist | Selected bradycardia / heart block | HR up while resistance and diastolic BP down; direct and reflex tachycardia |
| Dobutamine Adrenergic agonist | Predominantly β1 Direct agonist | Acute low-output failure; stress echo | Inotropy more than chronotropy; arrhythmia and ischemia risk |
| Albuterol Adrenergic agonist | β2 Direct agonist | Inhaled relief of bronchospasm | Tremor, tachycardia, hypokalemia; no steroid-like anti-inflammatory action |
| Amphetamine Indirect sympathomimetic | Indirect NE release Releases stored NE | ADHD; narcolepsy | Pairs with tyramine conceptually as NE-releasing agents |
| Tyramine Indirect sympathomimetic | Indirect NE release Releases stored NE | Food interaction example | MAOI plus tyramine can cause hypertensive crisis; not an antidepressant |
| Cocaine Indirect sympathomimetic | Indirect monoamine action Blocks NE reuptake and Na+ channels | Sympathomimetic and local anesthetic recognition | Vasoconstriction, ischemia, arrhythmia, seizures |
| Ephedrine Mixed-acting sympathomimetic | Direct + indirect Receptor activation plus NE release | Hypotension recognition | Noncatechol, COMT resistant; store depletion causes tachyphylaxis |
| Pseudoephedrine Mixed-acting sympathomimetic | Direct + indirect Receptor activation plus NE release | Decongestion | Noncatechol, COMT resistant; store depletion causes tachyphylaxis |
| Phenoxybenzamine Adrenergic antagonist | α1 + α2 blocker Irreversible blockade | Pheochromocytoma | Orthostasis and tachycardia; alpha block before beta block in pheochromocytoma |
| Phentolamine Adrenergic antagonist | α1 + α2 blocker Reversible blockade | NE extravasation; catecholamine excess | Orthostasis and tachycardia |
| Prazosin Adrenergic antagonist | α1 blocker Selective blockade | Hypertension; BPH | First-dose syncope; relaxes bladder outlet |
| Terazosin Adrenergic antagonist | α1 blocker Selective blockade | Hypertension; BPH | First-dose syncope; relaxes bladder outlet |
| Doxazosin Adrenergic antagonist | α1 blocker Selective blockade | Hypertension; BPH | First-dose syncope; relaxes bladder outlet |
| Tamsulosin Adrenergic antagonist | α1A blocker Subtype-selective blockade | BPH | Less BP effect than broader α1 blockers |
| Propranolol Beta blocker | β1 + β2 blocker Nonselective blockade | CV uses; tremor; migraine; adrenergic symptoms | Bronchospasm and bradycardia risk |
| Nadolol Beta blocker | β1 + β2 blocker Nonselective blockade | CV uses | Bronchospasm and bradycardia risk |
| Timolol Beta blocker | β1 + β2 blocker Nonselective blockade | Lowers aqueous production in glaucoma | Bronchospasm and bradycardia risk |
| Atenolol Beta blocker | β1 blocker Relatively selective blockade | CV uses | Selectivity is dose-dependent |
| Metoprolol Beta blocker | β1 blocker Relatively selective blockade | CV uses | Selectivity is dose-dependent |
| Esmolol Beta blocker | β1 blocker Relatively selective blockade | Short IV rate control situations | About 10-minute half-life |
| Labetalol Mixed alpha-beta blocker | α1 + β blocker Combined blockade | Hypertension | Blocks both vascular and cardiac sympathetic effects |
| Carvedilol Mixed alpha-beta blocker | α1 + β blocker Combined blockade | Stable HFrEF | Blocks both vascular and cardiac sympathetic effects |
| Pindolol Beta blocker with ISA | β blocker with partial agonism Partial agonist | Recognition example | Less resting bradycardia due to intrinsic sympathomimetic activity |
This section catches the remaining high-yield named drugs from the quick sheets so they are not omitted from your review resource even though they are not part of the autonomic core.
| Drug or class | Main target | Recognition hook |
|---|---|---|
| Aspirin | COX inhibition | Irreversible NSAID; GI/renal risks; high salicylate doses may saturate elimination |
| Ibuprofen | COX inhibition | Reversible NSAID; GI/renal risks |
| Cortisol / glucocorticoids | Intracellular receptor | Anti-inflammatory/immunosuppressive; chronic hyperglycemia, infection, osteoporosis, adrenal suppression |
| Heparin / protamine | Antithrombin enhancement / chemical antagonism | Protamine neutralizes heparin |
| Insulin | Receptor tyrosine kinase | Lowers glucose; drives K+ into cells |
| Omeprazole / cimetidine | H+/K+ ATPase / H2 receptor | Both lower acid; pump inhibitor versus receptor blocker |
| Nitroglycerin | NO → guanylyl cyclase → cGMP | Venodilation, angina, headache, hypotension |
| Ampicillin / vancomycin | PBPs / D-Ala-D-Ala | Cell-wall antibiotic recognition pair |
| Chloroquine / indinavir / felodipine | Heme detox / HIV protease / L-type Ca2+ channel | Recognition examples with PK/interactions |
| Procainamide / lidocaine | Na+ channel blockers IA / IB | Antiarrhythmic recognition; lidocaine also local anesthetic |
| Morphine / acetaminophen | Mu receptor / central analgesic-antipyretic action | Morphine causes respiratory depression and constipation; acetaminophen excess causes liver toxicity |
| Phenytoin / ethanol | Na+ channel stabilization / CNS depressant | Zero-order/capacity-limited elimination examples |
| Theophylline / phenobarbital / carbamazepine | PDE inhibition + adenosine antagonism / GABA-A enhancement / Na+ channel block | Theophylline narrow window; phenobarbital and carbamazepine induce CYP |
| Rifampin / erythromycin / chloramphenicol | Bacterial RNA polymerase / bacterial 50S / bacterial 50S | Major CYP interaction memorization set; chloramphenicol marrow toxicity |
| Bisphosphonates / chondroitin / antacids | Less osteoclast resorption / GAG supplement / acid neutralization | Structural or nonreceptor examples |
| Thyroid hormone / vitamin D / testosterone | Intracellular nuclear receptor signaling | Transcriptional regulation examples |
| Sulfonamides | Bacterial DHPS inhibition | Less folate synthesis; humans lack DHPS |
| Trimethoprim | Bacterial DHFR inhibition | Sequential block with sulfonamides |
| Methotrexate | Human DHFR inhibition | Less purine and dTMP synthesis; folinic acid bypasses DHFR |
| Mycophenolic acid | IMP dehydrogenase inhibition | Less GMP; transplant immunosuppression |
| 6-MP / azathioprine | Thiopurine activation via HGPRT | Purine synthesis inhibition; low TPMT causes myelosuppression |
| Hydroxyurea | Ribonucleotide reductase inhibition | Less DNA precursors; HbF rises in sickle disease |
| 5-Fluorouracil | Thymidylate synthase inhibition via FdUMP | Less dTMP; mucositis, diarrhea, marrow toxicity |
| Allopurinol / oxypurinol | Xanthine oxidase inhibition | Lower urate production |
| Febuxostat | Nonpurine xanthine oxidase inhibition | Lower urate production |
| Probenecid | Blocks renal urate reabsorption | Uricosuric; stone risk |
| Colchicine | Tubulin / microtubule inhibition | Reduces gout inflammation, not urate |
| Uridine | UMP salvage bypass | Treats hereditary orotic aciduria |
| Decitabine | DNMT inhibition after DNA incorporation | Hypomethylation and re-expression of silenced genes |
| Trastuzumab | HER2/ERBB2 antibody | HER2-positive breast cancer; cardiomyopathy risk |
| Imatinib | BCR-ABL kinase inhibition | Philadelphia-positive CML |
| Vinblastine / vincristine | Tubulin inhibition | Vinblastine marrow suppression; vincristine neuropathy |
| Cisplatin / irinotecan | DNA crosslinks / topoisomerase I inhibition | Cisplatin kidney-ear toxicity; irinotecan diarrhea plus marrow suppression |
This file inventory is included so you can verify the resource was built against both the attached documents and the broader FTM2 folder rather than from a single sheet alone.
Drug names, receptor summaries, and high-yield distinctions were structured from these two core attachments.
Use the page as a sequence, not just as a document.
Memorize M1, M2, M3, Nn, Nm, α1, α2, β1, β2, β3, and D1 by signal, location, and body effect. That gives you a prediction engine.
Compare look-alikes: bethanechol versus neostigmine, physostigmine versus neostigmine, phenylephrine versus epinephrine, tamsulosin versus prazosin, succinylcholine versus nondepolarizers.
Close with the recognition table and force yourself to say one target and one key risk for every named drug family on the sheet.