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Introduction to ANS Pharmacology Dr . Kaukab Azim + Dr. Hanin Osama

Introduction to ANS Pharmacology Dr . Kaukab Azim + Dr. Hanin Osama. NS. Central Brain Spinal cord Peripheral Afferent (sensory) Efferent (motor, autonomic ). ANS Regulates Involuntary Functions. Blood pressure Heart rate Respiration Body Temperature Glandular Secretion

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Introduction to ANS Pharmacology Dr . Kaukab Azim + Dr. Hanin Osama

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  1. Introduction to ANS Pharmacology Dr. KaukabAzim + Dr. Hanin Osama

  2. NS • Central • Brain • Spinal cord • Peripheral • Afferent (sensory) • Efferent (motor, autonomic )

  3. ANS Regulates Involuntary Functions • Blood pressure • Heart rate • Respiration • Body Temperature • Glandular Secretion • Digestion • Reproduction

  4. The ANS facilitates immediated physical reactions associated with a preparation for violent muscular action. • Acceleration of heart and lung action • Paling or flushing, or alternating between both. • Inhibition of stomach and upper intestinal action (digestion slows down or stops) • Liberation of nutrients for muscular action • Dilation of blood vessels for muscles • Inhibition of Lacrimal gland and salivation • Dilation of pupil

  5. III All preganglionic nerves secrete Ach. Ganglionic blocking drugs block transmission. (e.g.Mecamylamine) Ciliary III Pterygopalatine VII VII Submandibular VII IX X IX Otic T1 T1 X – Vagus T2 T2 T3 T3 T4 T4 T5 T5 T6 T6 T7 T7 Parasympathetic Sympathetic T8 T8 T9 T9 T10 T10 T11 T11 T12 T12 L1 L1 L2 L2 L3 L3 L4 L4 L5 L5 S1 S1 S2 S2 Pre-ganglionic Blue Pre-ganglionic Red S3 S3 Nervi erigentes S4 S4 Post-ganglionic Pink Post-ganglionic Green

  6. Location of cholinergic transmission • All autonomic ganglia • Voluntary muscles (neuromuscular junction) • Adrenal medulla (secretion of adrenaline) • Post ganglionic parasympathetic • Post ganglionic sympathetic to sweat glands

  7. Acetyl Choline (Ach) Synthesis: • At the nerve terminals • CAT (choline acetyl transferase), From Choline • 50% of it, is recaptured by nerve terminals

  8. Potential targets for drugs Five key features of neurotransmitter function provide potential targets for pharmacologic therapy: • synthesis, • storage, • release, • termination of action of the transmitter, • functions of the receptor.

  9. Parasympathomimetic

  10. Effects of Muscarinic agonists A. Cardiovascular system • Slow heart rate (negative chronotropy) • Decreases conduction velocity and increases refractory period • Bradycardia and vasodilatation lead to drop in BP • Vasodilatation of arteries and veins due to stimulation of M3 receptors in the endothelium, releasing NO

  11. Continue… B. RESPIRATORY • Bronchio-spasm • increase secretion C. GIT • Increase peristalsis • Increase secretions mainly salivary and gastric • Sphincters are relaxed

  12. Continue… D. GU • Stimulation of detrusor muscle and Relaxation of the trigone and sphincter of the bladder thus promote micturition. E. Eye • Causes contraction of the smooth muscle of the iris causing miosis and of the ciliary muscle (accommodation of near vision) • It will facilitate the outflow of aqueous humor into the canal of Schlemn which drains the anterior chamber

  13. Continue… F. Exocrine gland • Increased their secretion, sweating, lacrimation and salivation G. CNS • Ach is widely distributed in the brain • It is a excitatory neurotransmitter in the basal ganglia • Its effect include; increased locomotor activity tremor

  14. Nicotinic agonists • Peripheral nervous system • Activation of nicotinic receptors in the autonomic ganglia result in firing action potential in postganglionic neurons • The action is same on both sympathetic and parasympathetic ganglia

  15. B. NMJ • Application of nicotine agonist in NMJ leads to depolarization of the endplate • The response vary from fasciculation of independent motor units to a strong contraction of entire motor unit.

  16. MUSCARINIC ANTAGONIST • Atropine • Scopolamine • Ipratropium • Pirenzepine

  17. Pharmacological actionMuscarinic antagonist 1- CNS: • Atropine in therapeutic doses has a minimal stimulant effect on CNS and a slower-long lasting sedative effect on the brain • Scopolamine has more marked CNS effects producing drowsiness in recommended doses • In high doses scopolamine and to a lesser extent atropine causes agitation, excitement, hallucination and coma

  18. 2- eye: • Mydriasis • Cycloplegialeads to loss of accommodation of near vision (eye can not focus on near objects) • Reduction of lacrimal secretion, dry eyes

  19. 3- CVS: • The initial effect is bradycardiafollowed by tachycardia • The initial bradycardia is often with lower doses and is due to blockade of presynaptic M1 muscarinic receptors on vagal nerve, thus facilitate Ach release • The tachycardia is due to blockade of M2 receptors in the SAN • Therapeutic doses of atropine is abolishes peripheral vasodilatation induced by cholinomimetics.

  20. 4- Respiratory system: • Antimuscarinic drugs are added to general anesthetics to reduce secretion in the trachea 5- GIT • marked reduction in salivary secretion (dry mouth) • Gastric secretion is blocked less effectively.

  21. 6-GU: • Smooth muscle of the uterus is relaxed • Bladder wall is relaxed and voiding is slower 7- sweat glands • Sweat gland secretions are blocked by antimuscarinic drugs, thermoregulation is suppressed leading to increase in body temperature.

  22. Nicotinic antagonists A) neuromuscular blockers : 1- depolarizing NMJ blocking drugs;the depolarizing blockers first depolarize the motor end-plate and then prevent further depolarization. E.g. Succinylcholine 2- non-depolarizing NMJ blocking drugs; compete with acetylcholine for receptors at the neuromuscular junction and clinical relaxation begins when 80–85% of the receptors on the motor end-plate are blocked. tubocurarine

  23. Ganglion blocking drugs B. Ganglion blocking drugs can occur by several mechanisms: • By interfering with Ach release • By prolonged depolarization due to large dose of stimulation • By interfering with postsynaptic action of Ach.

  24. ADRENERGIC AGONIST & ANTAGONIST

  25. SYMPATHOMIMETICS Classification: A- According to the source: • Natural; NE, EP, DA • Synthetic; isoproternol, ephedrine, amphetamine B- chemically: • Catecholamines; NE, EP, DA and isoproternol • Non catecholamines; ephedrine, amphetamine, tyramine

  26. α1 found in the smooth muscle of many organs and they cause contraction of the blood vessels, relaxation of the GIT and glycogenlysis • α2 found in presynaptic neuron ,CNS, blood vessels , it inhibit transmitter release, in addition they cause platelets aggregation and blood vessel contraction. If found postsynaptically work as α1 • β1 mainly in the heart ,stimulation result in an increase cardiac out put and heart rate • β2 present in the smooth muscle of many organs and its stimulation lead to bronchodilation, perpherial vasodilation, relaxation of the visceral smooth muscle and skeletal muscle tremor

  27. PHARMACOLOGYCAL EFFECTS OF SYMPATHOMIMETIC 1- Cardiovascular system • The overall effects on blood vessels depend on the relative activities of the sympathomimetics at α or βreceptor. • α1; increase arterial resistance • β2 receptors promote smooth muscle relaxation • β1: Activity of both normal (SAN) and abnormal (purkinjefibers) is increased (positive chronotropic effects). • Contractility is increased (positive inotropic effects)

  28. 2. eye: • Activation by α1 agonist causes mydriasis • α1- agonists increases the outflow of aqueous humor from the eye, while β antagonists decreases the production of the aqueous humor. These effects are beneficial in treatment of glaucoma. 3. Respiratory • Activation of β2 receptors in the bronchial muscle results in bronchiodilatation.

  29. 4. GU • In human uterus the β2 receptors mediate relaxation that might be useful during pregnancy. • The bladder base, urethral sphincter and prostate contain α receptors that mediate contraction and therefore promote urinary continence. 5. effects on endocrine function • Insulin secretion is stimulated by β receptors and inhibited by α2 • Renin secretion is stimulated by β1 and inhibited by α2

  30. 6- Metabolic effect • Activation of β3 receptors in fat cells leads to increased lipolysis. • Sympathomimetics enhances glycogenolysis in the liver that leads to increased glucose release into the circulation (mediated mainly by β2) • Activation of β2 receptors promotes uptake of potassium into cells, leading to fall in extracellular potassium.. • Carbohydrates metabolism in the muscle and liver is enhanced

  31. α-blocker • Selective α1 (prazosin): • Vasodilation • Hypotension • Selective α2 (yohimbine) • Increase nor adrenaline release and cause sympathomimetic effect • Can block α2 in blood vessel and cause vasodilatation

  32. Non selective α-blockers • Phenoxybenzamine, phentolamine • Vasodilatation • Reduce blood pressure

  33. β-blocker • Non selective: • Propranolol, labetalol • Selective • Atenolol, metoprolol • Reduce HR (-vechronotropic) • Reduce force of heart contraction (-veionotropic)

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