Basics terms of autonomous nervous system (ANS)
Structure & gross level mode of signal transmission:
- At the synaptic region, axon of the first neuron makes synapse with - dendron/cell soma/axon of second neuron.
- At terminal part, axon of 1st neuron shows swelling and called presynaptic knob.
- Neurotransmitters are present in vesicles.
- Region between two neuron synapatic cleft (20nm).
- ANS ganglia : axodendric synapse.
- Anterior horn of spinal cord : axosomatic synapse.
- Neuromuscular junction is present between the motor nerve twig and the muscle cell.
- An axon of a motor nerve breaks up into many fine terminal twigs. Each such twigs supplies a muscle fibre.
- As twig approaches muscle fibre, it looses its mylein sheath and becomes swollen--> terminal bulb.
- The portion of the muscle fibre where terminal knob is impreganated -----> motor end plate(contains receptors).
- Subneurol cleft are present on motor end plate.
- EPP, assume at rest, potential of membrane = -90mV
- After lombination(2) = -65mV
- EPP(2-1) = +25mV
- Transmitter is always Ach and receptors are nicotinic (Nm)
c) Eneteric Nervous system:
- James Langley coined the term ENS (father of ANS physiology).
- There are two sets of local nerves are found in the gut wall-
- Auerbach’s (myenteric) plexus- between the longitudinal and circular layer of gut muscles.
- Meissner’s plexus- lies in submucons coat.
Some special issues about transmitters and transmissiona) Denervation supersensitivity:
If a nerve supplying the target organ (skeleton, smooth, myocardium) be cut, after some days it will be seen that application of the neurotransmitter to the target organ produces an usually strong effect.
Reasons : a) Increase in no. Of receptor. b) No reuptake as there will be no presynaptic membrane. c) Enhanced postreceptor binding effect.
Most organs receive dual supply of sympathetic and parasympathetic nerves. When one nervons system dominates, other suppresses.
Homotropic inhibition: Consider the example of norepinephrine (NE).
- There are two types of receptors: a) Presynaptic (responsible for release & reuptake) b) Postsynaptic (biological action).
- At low concentration of NE at synaptic cleft- NE binds with beta presynaptic receptors--> +ve feedback.
- Also, epinephrine released from adrenal medulla cause +ve feedback as it also binds with beta receptor.
- At high concentration NE binds with alpha receptor ---> -ve feedback (Reuptake). These presynaptic receptors are called autoreceptors.
Anatomy & Physiology of ANS
General introduction: The ANS has two divisions
Cannon, 1928 --------> sympathetic system ---------> fight or fight reaction
a) Anatomy of sympathetic nervous system:
|Sympathetic nervous system|
|Anatomy of sympathetic nervous system|
Receptors of sympathetic nervous system:
|Receptors of sympathetic nervous system|
b) Anatomy of parasympathetic nervous system (PNS):
|Receptors of PNS|
- Ach is formed from----> acetyl CoA + choline
- AcetylCoA is synthesized in mitochondria of synaptic knob.
- Choline is obtained by recycling. Acetyl CoA + Choline --------> Accetylcholine
- Ach synthesized in cytoplasm of synaptic knob and travels to vesicles and released.
- Ach is destroyed by acetylcholine esterase, AchE
|Classification of cholinergic drugs on the basis of mechanism of action|
|Classification of cholinergic drugs on the basis of receptor|
Pharmacological actions of cholinergic drugs:
M receptors are present:
a) M1-----> Brain
b) M2 -------> Heart
c) M3 -------> Smooth muscles of exocrine glands
Effects of antimuscranic drugs:
a) Bronchi-----> bronchodilation and decrease glandular secretion
b) Skin and sweat glands-------> increase temp. As no sweating
c) GIT-------> little effect due to ENS activity also.
d) Secretion-----> decrease salivary, gastric and other secretions
|Classification of Anticholinergic drugs|
- - Hexamethonium
- - Trimethaphan
- - Mecamylamine
- - Pempidine
|Neuromuscular blocking agents|
Mechanism of action of Neuromuscular blocking agents:
a) Non-depolarising agents: binds with Ach receptor -----> No depolarization-----> No action
b) Depolarising blockers: Binds with Ach R------> depolarization ------> contraction -----> as depolarising blockers degraded slowly, so contraction prolongs ------> there is no relaxation muscle goes for paralysis.
Effects of activation of different receptors in symapthetic nervous system:
- most vascular smoothe muscles (Constriction & increased BP)
- Arrecorus pilorum ( Piloerection)
- Dilator pupillae (Dilation)
- Liver (rat) - Glycogenolysis
- Platelet (Aggregation)
- Vascular smooth muscles ( Constriction)
- Prejunctional membrane of synapse (Reuptake)
- Heart (Stimulate)
- Kidney ( increased renin secretion)
- Posterior pituatory ( Increased ADH)
- Smooth muscles (bronchial- dilation, arterioles of skeletal muscles- vasodilation, uterus- relax)
- Liver (Man)- Glycogenolysis
- Adipose tissues (Lipolysis)
|Biosynthesis of catecholamines|
- Sympathomimetics are derivatives of β-phenyl ethyl amine
- N atom separated by 2 carbon atoms from benzene ring - increased sympathomimetic action.
- If N has alkyl group - β activity
- OH at 3 & 5 position- β2 activity
- OH group at β-carbon- β activity
Effects of α1 blocking: Vasodilation ( Decreased BP) ---> Tachycardia as compensatory mechanism.
- Phenoxabenzamine & Phentolamine- α1 & α2 (blockers) ---> Pheochromocytopenia.
- Prazocin & Trazocin- α1 (blockers) ----> to treat hypertention
- Labetolol- α, β, & β2 blocker ------> to treat hypertention
- Propanolol (Non selective) Hypertention, Angina, Arrhythmia, Thyroid, AMI
- Atenolol & Metoprolol (β1) Hypertention, Angina, Arrhythmia, Thyroid, AMI
- Timolol (Non selective) Hypertention, Angina, Arrhythmia, Thyroid, AMI, Glaucoma
- Esmolol (β1) Supraventricular tachycardia
- Nadolol (Non selective) Hypertention, Angina
- Acebutolol (β1) Angina, Arrhythmia
- Pindolol (Non selective) Angina, Arrhythmia