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Pharmacology (Subject) / ANS (Lesson)

Part I

This lesson was created by Lydiamarieluise.

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  • Effecs Sympathetic<-->Parasympathetic nervous system Sympathetic                              <-->                 Parasympathetic Heart rate (+)                                                    Heart rate (-) Constriction blood vessels Gut motility (-)                                                    Gut motility and gastric acid secretion (+) Pupils dilate.                                                       Pupils constrict  Salivary glands (+) Gluconeogenesis + glycogenesis 
  • Transmission ganglion (sympathetic + parasympathetic) Stimulation efferent pre-ganglionic neuron --> Release ACh --> Type I nicotinic receptor --> Stimulation of post-ganglionic neuron --> Nicotinic type II receptors used in the SNS at neuromuscular junctions (different 5 subunits but same mechanism)
  • Transmission post-ganglionic nerve endings (Parasympathetic) stimulation Pre-ganglionic neuron --> Release ACh --> Muscarinic receptor --> Tissue
  • Transmission post-ganglionic nerve endings (Sympathetic) 1. MOST (!) - Pre-ganglionic neuron --> Noradrenaline --> Adrenergic receptor --> Tissue 2. Sweat glands  - Pre-ganglionic neuron --> ACh --> Mucarinic receptor --> Sweat gland 3. Adrenal medulla - NO ganglion, only one neuron from the thoracic region of the CNS --> ACh --> nicotinic type I receptor --> Adrenal Medulla --> release noradrenaline + adrenaline
  • Synthesis/Release/Breakdown of ACh (Process) + synapses using ACh as neurotransmitter 1. Stimulation of pro-synaptic neuron 2. Fusion of ACh granules with membrane --> Diffusion of ACh into synaptic cleft 3. Interaction with nicotinic (NMJ) or muscarinic receptors 4. Breakdown of ACh by acetylcholinesterase (AChE) 5. Reabsorption of Cholin into pre-synaptic nerve terminal and acetylation --> post-ganglionic parasympathetic nerve endings (efferent) use ACh as neurotransmitter, Sympathic post-ganglionic nerve ending (sweat glands) 
  • Drugs mimicking/blocking ACh at the muscarinic receptors 1. Mimicking ACh a) Pilocorpine - eye drops to treat glaucoma b) Bethonoecol - stimulates muscle contraction (urinary retention, return of normal GI function after anaesthesia) 2. Blocking ACh a) Atropine - reduces secretion (before surgery) b) Ipatropium - brochodilator (asthma, COPD) c) Hyoscine - motion sickness or to facilitate endoscopy d) Tropicamide - eye dilation
  • Drugs acting on ACh at NMJs - use ACh too, but with nicotinic type II receptors --> only drugs acting on synthesis/release/metabolism of ACh affect the SNS as NMJs habe no muscarinic receptors 1. Drugs preventing ACh release a) Botulinum toxin - inhibits release of ACh (used to treat dystonia) 2. Drugs affecting AChE a) Anticholinesterases (short acting) -  diagnosis of myasthenia gravis (edrophonium) b) Anticholinesterases (medium duration) - treatment of myasthenia gravis (neostigmine) c) Anticholinesterases (irreversible) - in pesticides and poisin gases (Sarin)
  • Synthesis/release/Removal Noradrenaline (Process) 1. Uptake of tyrosine by the pre-synaptiv neuron --> convertion to NA 2. Stimulation of pre-synaptic neuron 3. Release of NA into the synaptic cleft 4. Interaction with adrenergic receptors on post-synaptic target tissue  5. NA in the synaptic cleft is either taken up into the pre-synaptic cell and metabolised by monoamine oxidase (MAO) or by neighbouring cells and metabolised by calechol O-methyl transferase (COMT)
  • Drugs blocking NA synthesis/reuptake/metabolism 1. Synthesis/Re uptake a) Reserpine - blocks packaging of NA into granules b) Amphetamine - displaces NA from the granules c) Cocaine and some antidepressants - block the reuptake of NA from the synaptic cleft   2. Metabolism a) MAO inhibitors (antidepressants)  b) COMT inhibitors (Parkinson's disease) - prevention of dopamine breakdown
  • Drugs mimicking/blocking the actions of NA on the sympathetic nervous system 1. Mimicking (Symphomimetics) a) Salbutamol - bronchidilator (asthma) b) Adrenaline - added to local anaesthetics to reduce diffusion, cardiac arrest c) Dobutamine - stimulates heart 2. Blocking (Sympholytics) a) Propranol (b-blocker) - angina, hypertension, anxiety  b) Prazosin - hypertension, benigh prostate hypertrophy
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  • Action of NA/A on peripheral adrenoceptors - not only sympathetic nerve endings release NA but also the adrenal medulla (NA+A) after activation by ACh 1. a-subtype a) a1-subtype - blood vessels, smooth muscle b) s2-subtype - pre-synaptic cells (inhibit the release of neurotransmitter) 2. b-subtype a) b1-subtype - heart (increaese rate and force of contraction) b) b2-subtype - bronchial and uterine smooth muscle --> A is a potent stimulus for a-and b receptors  --> NA is a potent stimulus for a receptors but less effective on b receptors

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