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Theory-Pharmacology-BDS
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ANS Introductio
n
Dr.U.P.RathnakarMD.DIH.PGDHM
ANS-PharmacologyNervous systemSympathetic and ParasympatheticFunctions and ConnectionsReceptors –Symp[Adrenergic] &
P.Symp[Cholinergic]NeurotransmittersNeurotransmissionCholinergic agonists and antagonistsAdrenergic agonists and antagonists
Motor
Sensory
Enteric
Neuronal connections-Somatic & ANS
Autonomic Somatic
Supplies all innervated Sk.Muscles structures
Synapses outside CNS Inside C.S.axis Ganglia No ganglia
Peripheral plexus + Absent Post ganglionic fibres Post ganglionic fibres
non-myelinated myelinated
Spontaneous activity Nil
in effectors
Interruption of nerve supply Disuse Atrophy
-no atrophy
NA and Adrenaline Acetylcholine
Flight, Fight and Fright Sit & Digest
Sympathtic P.Sympathtic
Organ Sympathtic P.Sympathetic [Flight & Fright] [Sit & Digest]
Survival Possible Not possible Eye MydriasisMiosis Heart Stim. Dep. Bronchi Dilation Spasm GIT ↓Motility ↑Motility ↓Secretion ↑SecretionContracts spincter Relaxes spincters UB Relaxes detrusor Contracts detrusor, Contracts trigone Relaxes trigone &
& spincter spincter
Sexual organs Ejaculation Erection
Sk.MusclesContractility increased
Adrenergic receptors[Symp]Receptors: α1a, α1b, α1d,
α 2a α2b α2c
β1, β2, β3
Neurotransmitter- Nor adrenaline, Adrenaline
Receptors- ParasympetheticCHOLINERGIC
Muscarinic= M1, M2, M3, M4, M5
Nicotinic= NN, NM
Neurotransmitter = Acetylcholine
Neurohumoral transmission“ Nerve impulses elicit responses in effector organs and post synaptic neurones through liberation of specific chemical transmitters”
Junctional transmission Vs Nerve conduction
History: Neurotransmission
Initially thought tobe electrical.
Otto Lewi → Frog hearts perfused in series →
Stim.vagosymp.trunk of I organ
→Perfusate produced inhibitory effect on II heart. →
Vagus stoffe. ( Acceleran stoffe.)
Tachycardia or Bradycardia
TachycardiaOr Bradycardia
Otto Lewi’s experiment
Flow of Chemic
alsubstan
ce
Otto Lewi’s Expt
Criteria: NeurotransmitterShould be present in
Presynaptic neurones
Should be Released on nerve impulse
Application of sub. Produces Similar response to nerve stimulation
Effects are antagonised or
potentiated by other sub. Which also similarly alter nerve stimulation.
Steps in neurotransmission: Impulse conductionArrival of impulseSynthesis Storage & release
of transmitter
Combination of transmitter
with P.J. receptors
Postjunctional activity: Excitatory[EPSP] or Inhibitory[IPSP]
Termination of neurotransmitter action
[Diffusion, destruction, reuptak
Impulse conduction:
Arrival of impulse→ ↑ Na conductance→ Depolarization→Inside (+)ve→(K flows out→Repolarization) →Action potential→Impulse propogation.
Storage & release of transmitter:
Neurotransmitter synthesized and stored in pre junctional nerve endings in “Synaptic Vesicles”
Arrival of nerve impulse→Fuses vesicular and axonal membrane(small amounts constantly released without impulse)
Ca entry fluidizes membrane→Contents of vesicle released→Exocytosis
Other protiens also participate in docking and fusion.
Presynaptic receptors modulate transmitter release
Combination of transmitter with P.J. receptors and P.J.potential:
Excitatory post synaptic potential(EPSP): ↑ permeability to cations-Na or Ca→ Depolarization→ EPSP
IPSP: ↑ permeability to K or Cl→ Hyperpolarization→ IPSP
Postjunctional activity: EPSP more than threshold level
→AP→ActivityIPSP(neurones, smooth muscles not in
Sk.muscles) → Opposes excitatory impulses
Final response depends on summation of all responses
Termination of neurotransmitter action:
Dissipation or destructionACHE(acetylcholinesterase) →Hydrolyzes Ach. →if ACHE is inhibited action prolonged
Adrenergic- Diffusion, Reuptake
NON-Electrogenic functions of neurotransmitter:
Continuos low grade release→No P.J. activity→ But imp. For turn over of enzymes of synthesis, inactivation, maintainance of pre and post synaptic transmission. These are trophic actions of neurotransmitter.
Co-Transmitter: Other transmitters released along with principal transmitter
Ach-VIP, NA-ATPOther cotransmitters- Adenosine,
neuropeptide-Y, NO, Somatostatin etc. NANC: Nonadrenergic-noncholinergic
transmission-exists in ANS. Principal transmitter is not Ach or NA. Eg. In GIT, GUT, (adenosine, ATP)
NN
NM
M1 M2 M3
α1α2
β1β2β
3
NN
NN
α1α2
β1β2β
3