🧬 ANS Anatomy & Ganglia

  • overview Autonomic nervous system (ANS) – involuntary control of viscera, heart, vessels, glands
  • Two major divisions:
    • Parasympathetic (PANS) – rest & digest, craniosacral outflow
    • Sympathetic (SANS) – fight or flight, thoracolumbar outflow
  • Ganglia location:
    • SANS ganglia – paravertebral chains (close to spinal cord)
    • PANS ganglia – within or near effector organs (intramural)
  • Somatic nervous system: no ganglia; single motor neuron from CNS to skeletal muscle
  • Preganglionic fibers: all release ACh (both PANS & SANS)
  • Postganglionic fibers:
    • PANS – ACh at muscarinic receptors
    • SANS – mostly NE at adrenoceptors (except sweat glands – ACh)
CNS → preganglionic (ACh) → ganglion (NN) → postganglionic (NE / ACh) → effector

⚡ Neurotransmitters

  • Acetylcholine (ACh)
    • All preganglionic fibers (PANS & SANS)
    • All postganglionic PANS fibers
    • Somatic motor neurons (NMJ)
    • Adrenal medulla (preganglionic cholinergic)
  • Norepinephrine (NE)
    • Major postganglionic SANS transmitter
    • Acts on α & β adrenoceptors
    • In cardiac & smooth muscle
  • Epinephrine (E)
    • Adrenal medulla – released into blood
    • Activates most adrenoceptors (α1, α2, β1, β2)
  • Dopamine (DA)
    • D₁ receptors in renal & mesenteric beds → vasodilation
    • Precursor to NE & E
Key: ACh is the primary transmitter at all autonomic ganglia and the neuromuscular junction.

🎯 Receptor types – location & function

ReceptorLocationEffector
NN nicotinicAutonomic ganglia (PANS/SANS), adrenal medullaDepolarization → ganglionic transmission
NM nicotinicSkeletal muscle motor end plateMuscle contraction
M1–M3 muscarinicEffector organs (PANS postganglionic), sweat glands (SANS)Variable: bradycardia, secretion, smooth muscle contraction
  • Adrenoceptors (α₁, α₂, β₁, β₂, β₃) – bind NE / E
  • α₁ – vasoconstriction, mydriasis, bladder sphincter contraction
  • β₁ – cardiac: ↑ rate, ↑ contractility, ↑ AV conduction
  • β₂ – bronchodilation, vasodilation (skeletal muscle), uterine relaxation

🔄 Neural feedback – baroreceptor reflex

  • BP = CO × TPR (cardiac output × total peripheral resistance)
  • Baroreceptors in carotid sinus & aortic arch sense mean arterial pressure
  • ↑ BP
    • ↑ baroreceptor firing → ↑ PANS outflow
    • ↓ SANS outflow
    • ↓ heart rate (bradycardia), ↓ contractility, ↓ CO
    • ↓ TPR (vasodilation) → BP returns toward normal
  • ↓ BP
    • ↓ baroreceptor firing → ↓ PANS, ↑ SANS
    • ↑ HR, ↑ contractility, ↑ CO
    • ↑ TPR (vasoconstriction) → BP rises
  • Blockade points:
    • Ganglionic (NN) antagonists → block reflex arc
    • Muscarinic antagonists → block reflex bradycardia
    • β₁ antagonists → block reflex tachycardia
↑ BP→baroreceptor ↑→↑ PANS / ↓ SANS→↓ HR, ↓ CO, ↓ TPR

🧪 Hormonal feedback – renin-angiotensin

  • Activated primarily by ↓ renal perfusion pressure (hypotension)
  • Juxtaglomerular cells → release renin
  • Renin converts angiotensinogen → angiotensin I
  • ACE (angiotensin-converting enzyme) → angiotensin II
  • Angiotensin II effects:
    • Potent vasoconstriction → ↑ TPR
    • Stimulates aldosterone release → Na⁺/H₂O retention → ↑ blood volume
    • ↑ venous return → ↑ CO
  • Net effect: restore BP via ↑ CO and ↑ TPR
Clinical trap: antihypertensives may trigger compensatory tachycardia and fluid retention via these feedback loops.

💊 ANS drug effects – eye & cardiovascular

  • Muscarinic agonists (e.g., pilocarpine)
    • Miosis (pupillary constriction)
    • Accommodation for near vision (ciliary muscle contraction)
  • Muscarinic antagonists (e.g., atropine)
    • Mydriasis (pupil dilation)
    • Cycloplegia – paralysis of accommodation (far vision)
  • α₁-agonists (e.g., phenylephrine)
    • Mydriasis (radial iris muscle contraction)
    • No cycloplegia (ciliary muscle unaffected)
  • β₁-blockers – ↓ HR, ↓ contractility (used in hypertension, angina)
  • α₁-blockers – vasodilation, ↓ TPR
Drug classPupilAccommodation
Muscarinic agonistMiosisNear vision
Muscarinic antagonistMydriasisCycloplegia (far)
α₁-agonistMydriasisNo cycloplegia

🩺 Clinical pearls & exam points

  • Baroreceptor reflex can be overridden by drugs:
    • Ganglionic blockers (NN antagonists) – abolish reflex
    • Muscarinic blockers – prevent reflex bradycardia
    • β₁ blockers – prevent reflex tachycardia
  • Compensation with antihypertensives:
    • Vasodilators → reflex tachycardia (β₁-blocker often added)
    • Diuretics → renin-angiotensin activation (ACE inhibitor added)
  • Ocular pharmacology – differentiating mydriasis:
    • Atropine (muscarinic antagonist) – mydriasis + cycloplegia
    • Phenylephrine (α₁ agonist) – mydriasis, no cycloplegia
  • Autonomic tone – resting state has dominant PANS tone (heart, GI)
  • SANS activation: ↑ HR, ↑ BP, bronchodilation, glycogenolysis
High-yield: ACh acts at ALL autonomic ganglia (NN) and NMJ (NM) – always depolarizing.
Exam trap: Sweat glands are sympathetic but cholinergic (muscarinic) – so atropine blocks sweating.