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CHEMICAL TRANSMITTERS

CHEMICAL TRANSMITTERS. DEFINITION : it is the substance which transmits the nerve impulse from pre - synaptic to post - synaptic membrane . MECHANISM : Arrival of nerve impulse to Pre-synaptic membrane → causes Ca+ uptake by acetyl choline vesicles

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CHEMICAL TRANSMITTERS

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  1. CHEMICAL TRANSMITTERS DEFINITION : it is the substance which transmits the nerve impulse from pre - synaptic to post - synaptic membrane . MECHANISM : Arrival of nerve impulse to Pre-synaptic membrane → causes Ca+ uptake by acetyl choline vesicles → causes swelling and rupture of vesicles → causes release of acetyle choline which can cross the synaptic cleft → formation of acetylcholin - receptor complex → Increase Na permeability → Depolarisation Action potential This Causes Propagation of Nerve Impulse

  2. TYPES OF NERVE ENDINGSADRENERGICCHOLINERGIC(nor adrenaline)(ac . choline) I) Cholinergic neurotransmission :- ( six steps ) 1- Synthesis of acetyl choline :-( In cytoplasm) choline + acetyl CoA CAT Ach + CoA. ( choline - acetyl - transferase) 2- Storage of acetyl choline in vesicles In the synaptic vesicles . 3- Release of Acetyl choline :- Ca++ channels in the presynaptic membrane opens → Ac.ch. release by exocytosis 4- Binding to receptors . 5- Degradation of Ac.ch. choline Ac.ch. choline + acetate esterase 6- Recycling of choline Into the neurone for resynthesis of Ac .ch.

  3. SITES OF RELEASE OF ACETYL CHOLINE 1- Autonomic ganglia (i.e all preganglionic fibers) 2- All parasympathetic post - ganglionic fibers . 3- Some sympathetic post - gangljpnic as sweet glands and blood vessels of skeletal muscles. 4- M.E.P = motor end plate (i.e neuro - muscular junction) 5- Adrenal medulla (pre ganglionic ) 6- C.N.S .

  4. TYPES OF CHQLINERGIC RECEPTORS :

  5. A) Muscarinic receptors Sites : In cardiac muscles, smooth muscle and exocrine glands . Subtypes : Ml , M2 , M3 and M4 . 3-Some sympathetic post-ganglionic as sweet glands and blood vessels of skeletal muscles. 4- M.E.P = motor end plate (i.e neuro - muscular junction) 5- Adrenal medulla (pre ganglionic ) 6- C.N.S . Ml : in autonomic ganglia, CNS and gastric mucosa M2 : in cardiac cells and smooth muscles . M3 : in smooth muscles and secretory glands . M4 and M5 : unknown sites .

  6. Functions of muscarinic receptors : - It has prolonged reseponse, lasts for seconds, either exitation or inhibition :- 1- Cardiac inhibition ( slow heart rate.) 2- Broncho-constriction . 3- Salivary secretion 4- Increases G.I.T secretion and motility. 5- Pupillary constriction . 6- Contraction of ciliary muscle. 7- Contraction of urinary bladder and rectum .

  7. B) Function of Nicotinic Receptors :- It has short timed receponse only exitatory : 1- Help ganglion transmission . 2- Secretion of epinephrine and nor-epinephrine from Ad. Medulla. 3- Stimulates N.M.J (MEP) to produce skeletal muscle contraction

  8. FATE (REMOVAL) OF AC CHOLINE .By choline-estrase enzyme 2 types. True pseudo (false) - present in nerve –endings - present in plasma. • specific only for Ac - non specific, can act on • any ester - highly potent (strong) - less potent.

  9. PARASYMPATHOMIM ETIC DRUGS Acts By Two Ways : A) Direct : on tissues as muscarine, nicotine in small dose and carbachol. B) Indirect : anticholinesterases as DFP and Eserine (war gas)

  10. Anti cholinesterases : Two types : a) Reversible :- short acting e.g Eserine : generalized i.e. ↑ both muscarinic and nicotinic actions. Prostigmine: Nicotinic i.e ↑ skeletal muscles MEP activity = used in treatment of myasthenia gravis . b) Irreversible :- long acting drugs i.e toxic, called nerve gases, or insecticides as DFP which causes paralysis of motor functions → difficulty in breathing → death

  11. PARASYMPATHOLYTIC DRUGS Mechanism of action : 1) Persistent depolarization 2) Competitive inhibition as curare. Types : A) ganglion blockers - Nicotine in large doses - Hexamethonium They cause paralysis of autonomic ganglia by persistant depolarization . B) post - ganglionic blockers -Atropine C) MEP blockers - Curare - Botulinum - Flexidil - Succinyl cholin ( persistent depolarization)

  12. Curare :- acts by competitive inhibition to Ac.ch . It can be used together with succinyl choline as muscle relaxants ATROPINE (anti-muscarinic drug ): ACTION : a) ON THE EYES :- Mydriasis and cycloplegia(loss of ability for near vision) b) ON SALIVARY GLANDS :- Dryness of mouth c) ON G.I.T :- Decrease motility = antispasmodic d) ON RESPIRATION : - Block secretions in respiratory tract e) ON C.V.S :- Tachycardia = ↑ heart rate . f) ON URINARY TRACT :- ↓ motility of urinary bladder .

  13. Effect of injection of Ac.ch. after Atropine on A.B.P: Nicotinic receptors in adrenal medulla unblocked rise in A.B.P CLINICAL USES OF ATROPINE 1- Fundus examination → Mydriasis 2- Bronchial asthma → Bronchodilatation . 3- Treatment of colic →↓ motility of G.I.T . 4- pre anaethetic drugs to prevent cardiac arrest. 5- Befor surgery → to block respiratory secretions

  14. ADRENERGIC TRANSMISSION 5- STEPS :- Hydroxylase enz. 1- Tyrosine DOPA (In cytoplasm). Dopa dopamine . 2- Storage of nor epinephrine in vesicles :- OH Dopamine Nor. epinephrine ( In synaptic vesicles .) N.B In adrenal medulla only: CH3 Nor - epinephrine epinephrine . 3- Release of nor-epinephrine :- Into the synapse. 4- Binding by receptors : either post-synaptic ( on the effector organ) or pre- synaptic receptors ( on nerve endings.) 5- Removal of nor- epinephrine ( Fate ) .

  15. SITES OF RELEASE OF CATECHOLAMINES : 1- Adrenergic endings :- only nor - adrenaline . 2- Adrenal medulla :- causes release of : 80% epinephrine 20% nor-epinephrine FATE OF CATECHOLAMINES: 1- Active reuptake = 80-90% back into ad. vesicles. (Na-k Atpase sys.) 2- Destruction = 7 % by MAO (oxidation) COMT (methylation) 3- Excretion as such = 3 %

  16. ADRENERGIC RECEPTORS (ALQUISTE) α1 : STIMULATORY a) V.C b) stimulation of sphincters . α2 :- INHIBITORY 0 a) relaxation of walls of G.I.T b) pre - synaptic inhibition of release of nor epinephrine (-ve feedback) βl :- STIMULATORY (+) a) heart +ve increase H.R & contraction b) adipose tissue = lipolysis c) renin - angiotensin . system = ↑ ABP. β2 :-INHIBITORYO (–)relaxation of smooth muscles in : 1- bronchi = bronchodilatation . 2- blood vessels = V.D in skeletal blood vessels & coronaries.

  17. N.B β1 receptors are stimulated equally by epinephrine and nor- epinephrine B2 receptors stimulated more by epinephrine than N.E β2 adrcnoreceptors : tow groups α 1 & α2: αl receptors have high affinity for phenyl-ephrine present on post.synaptic membrane of effector organ . α2 receptors have high affinity for clonidine. present on Pre-synaptic nerve endings to control release of nor-epinephrine (causes its inhibition). N.B β2 pre-synaptic receptors stimulate NE release, both a 2 and β2 receptors are called pre - synoptic receptors.

  18. RECEPTOR STIMULANTS : α Receptors stimulated by : nor - adrenaline ]- adrenaline} isoproterenol β Receptors stimulated by : isoproterenol J. adrenalin]- nor - adrenaline N.B nor - adrenaline, has a more pressor effect because it acts mainly on α due to receptor sensitivity. RECEPTOR BLOCKERS : α Blockers : ergot alkaloids . β Blockers : inderal .(Propranolol.) N.B In G.I.T inhibition of the wall is by α2 and may be β2 receptors. While stimulation of sphincters only by al receptors (not β1 ). N.B α is stimulatory except on G.I.T, it is inhibitory While β is inhibitory except on heart, it is stimulatory.

  19. COMPARISON BETWEEN a & B RECEPTORS

  20. MECHANISM OF ACTION OF ADRENERGIC RECEPTORS αl Increases intra-cellular C-AMP. α2 Inhibit adenyl cyclase enzyme, so it decreases cyclic AMP so interfering between the combination between the transmitter and its receptor βl receptors stimulates adenyl cyclase , increases cyclic AMP β2 receptors → unknown mechanism but may also act by increasing C-AMP

  21. Sympathomimetic drugs (adrenergic Agonists ) Mechanism Of Action: 1- stimulate release of catecholamines e.g Tyramine ↓ (indirect acting agonist ) 2- inhibit reuptake e.g Cocaine 3- α stimulants Direct acting agonist 4- β stimulants

  22. SYMPATHOLYTIC DRUGS 1- Inhibit synthesis and storage e.g reserpine . 2- Inhibit release of catecholamines e.g guanithidine . 3- Recepor blockers a & B receptors 4- False transmiters e.g a methyl dopa( aldomet ). 5- Ganglion blockers e.g hexamethonium and arfonad

  23. DIFFERENCE BETWEEN

  24. PHEOCHROMOCYTOMA * Tumour of adrenal medulla resulting in attacks of hypertension in emergency states, discharge of sympathetic leading to: 1- increased arterial pressure 2- increased blood flow to active muscles 3- increased blood glucose level 4- increased rate of blood coagulation . 5- increased mental activity 6- increased glycogenolysis in liver and muscles . 7- increased rate of cellular metabolism.

  25. Control of A.N.S by Higher centers 1- Some autonomic reflexes as micturation, defecation and erection are under inhibitory control of centers in C.N.S . 2- Cardio-vascular, respiratory and digestive activity are under control of medulla within the brain stem. 3- Stimulation of anterior nucleus of hypothalamus is accompanied by parasympathetic effects, while stimulation of posterior nucleus is accompanied by sympathetic effects.

  26. 1- Cardiovascular autonomic reflexes :- High arterial pressure → baro-receptors → pressure fall back toward normal. 2- Gastrointestinal autonomic reflexes :- a) Un-conditioned reflex e.g. presence of food in mouth causing salivary secretion . b) Defecation reflex. c) Micturation reflex. d) Sexual reflexes : Erection (parasympathetic function, followed by ejaculation (sympathetic function) N.B biofeedback research demonstrate that the A.N.S is not autonomic, it can be voluntary.

  27. DISORDERS OF AUTONOMIC FUNCTIONS SYMPATHETIC QVERACTIVITY:- 1- HYPERTENSION :- sympathetic increases peripheral resistance 2- ANGINA PECTORIS :- sympathetic increases myocardial O2 3- Hyperthyroidism: Thyroid hormone increases sensitivity or number of adrenergic receptors

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