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Α-Adrenergic Antagonists

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α-Adrenergic Antagonists Objectives: ❖ Outline the mechanisms of action of adrenergic neuron blockers. ❖ Classify α-receptor blockers into selective & non -selective. ❖ Know the pharmacokinetic aspects & pharmacodynamic effects of a adrenergic blockers. ❖ Identify the specific uses of non-selective & selective α-adrenergic blockers. Important In male and female slides helpful video Only in male slides Only in female slides Extra information Editing file If you memorize this very well, you will be able to guess the pharmacological actions just by knowing the receptor of the drug. Post-synaptic (located in the tissue) α1 β2 β1 β3 Excitatory function Inhibitory in function In adipose (they cause contraction) (cause relaxation) Excitatory in function tissue ﻧﻔس ﻣﻛﺎن α1 ﻟﻛن ﻋﻛﺳﮭﺎ ﺑﺎﻟوظﯾﻔﺔ (except in GIT (inhibition Present mainly in heart, juxtaglomerular cells of Present mainly in smooth muscles the kidney (discussed later with renin) Relaxation of the uterus Contraction of uterus (Delay premature labor) (helps with delivery) (The 2nd baby is coming.)* * راح أﺟﮭض طﻔﻠﻲ اﻷولα1 (ﻗﻠﺑﻲ ھو ﺑﯾﺗك (اﻷول ↑ Heart rate: Vasoconstriction of skin & Chronotropic effect peripheral blood vessels (Tachycardia) →increased peripheral relaxations = ھذا ﺑﯾﺗك اﻟﺛﺎﻧﻲ ارﺗﺎح resistance (resistance to blood flow due ↑ Force of contraction : Relaxation of skeletal & coronary to constriction of blood vessels)→ inotropic effect ( Contraction of blood vessels (vasodilatation) ventricles & Increase cardiac output) hypertension. ↑ Conduction velocity: ↑ lipolysis dromotropic effect Pulse is conducted faster causing ↑ free fatty Relaxation Of GIT muscles (constipation) & Urinary bladder tachycardia acids muscles. ↑ Blood pressure Contraction Of GIT sphincter & urinary bladder sphincter ↑ (urinary retention) Renin release Enzyme released by the juxtaglomerular cells of the kidneys in response to low blood Contraction of radial muscle -Relaxation of bronchial smooth pressure, causing the of eye causes active mydriasis muscles (bronchodilation). transformation of angiotensinogen (dilation of pupil, cholinergic agents have no to angiotensin I which in turn effect on this muscle) -Tremor of skeletal muscles stimulates release of aldosterone (Which Causes vasoconstriction & BOTH Increase blood glucose level (hyperglycemia) either by: increases BP). This is useful during hemorrhaging to conserve blood ↑ glycogenolysis ↑ glucagon release from pancreas So hyperglycemia ↑ liver & muscle glycogenolysis Pre-synaptic (Regulation of Noradrenaline release) α2 β2 Inhibition of norepinephrine release Increase of norepinephrine release (Negative feedback mechanism) (Positive Feedback mechanism) This feedback decreases NE when it’s elevated This feedback increases NE when its levels are low a2 =(at)wo b2=(PT))wo 1-Alpha adrenergic blockers & sympatholytic Overview Non-selective (α1, α2) e.g phentolamine α-adrenergic receptor Selective α1 blockers e.g Prazosin Selective α2 Adrenergic receptor β-adrenergic receptor e.g yohimbine blockers blockers α & β -adrenergic receptor blockers (Sympatholytics) Adrenergic depressants Adrenergic Adrenergic neuron Formation of false e.g α-methyl dopa blockers transmitter Depletion of storage sites e.g Reserpine Inhibition of release & e.g Guanethidine enhance uptake Stimulation of presynaptic e.g clonidine & α2 receptors α-methyl dopa Adrenergic neuron blocker drugs Overview of what goes on inside nerve terminals: Tyrosine turns into Dopa ⟶ Dopa turns into Dopamine ⟶ Dopamine is stored in vesicles ⟶ inside vesicles dopamine turns into norepinephrine ⟶ release of norepinephrine to the synaptic space is stimulated by an action potential - Team 439 RESPA block Adrenergic neuron blockers act by inhibition of 1. The release of NE 2. The storage of NE 3. The synthesis of NE Reserpine Interferes with NE Clonidine α-methyldopa False Inhibition of Stimulation of Depletion “reduction and decreasing” presynaptic neurotransmitter release it of stores α2-receptors formation (Storage) (Release) negative feedback (Synthesis) α-methyldopa Guanethidine Adrenergic neuron blocker drugs Drug α -methyl dopa Clonidine Apraclonidine ﻣﯾﺛﺎء دوﺑﺎ ﻷﻧﮭﺎ ﺣﺎﻣل -Forms false transmitter that is -Central α2 receptor Acts by decreasing released instead of NE. agonist acts on brainstem aqueous humor “α-methylnoradrenaline replaces NE in vesicles” to inhibit NE release. formation. -Centrally acting α2 adrenergic (negative feedback) “Aqueous humor maintain agonist that inhibits NE release. -Suppresses sympathetic intraocular pressure” Extra info: Instead of forming NE from dopamine, α-methyl outflow activity from the dopa will form a false neurotransmitter known as brain. “Decrease of sympathetic α-methylnoradrenaline which replaces NE in outflow to the heart and blood vessels vesicles. This false neurotransmitter will stimulate cause decrease in blood pressure” α2 receptors that will decrease the release of NE M.O.A (negative feedback). -Drug of choice in treatment of -Little use as an hypertension in pregnancy antihypertensive drug as (gestational hypertension sudden discontinuation Open angle glaucoma Uses pre-eclampsia). “disorder of pregnancy can cause rebound as eye drops (topical) characterized by proteinuria and rise in BP” hypertension due to a As it has no teratogenic effect rebound in sympathetic ”ﻻ ﯾﺳﺑب ﺗﺷوه أﺟﻧﺔ” outflow. Adrenergic receptors blockers Classification of α-receptor antagonists Non-Selective α Selective α1 antagonists Selective α2 antagonist adrenoceptor e.g. e.g. e.g. ● Phenoxybenzamine ● Prazosin ● Yohimbine ● Phentolamine ● Doxazosin ● Tamsulosin (α1A ) ”more selective α1 antagonist” Non-selective α-receptor blockers Drug Phentolamine Phenoxybenzamine α α M.O.A Non-selective antagonists of both 1 and 2 receptors. ● Reversible block both α1 and α2 ● Irreversible blocking of α1 and receptors.(shift to the right) α2 receptors.(No parallel shift) “By “Non-covalent bond so less duration of action” covalent bond” ● Short acting ( 4hrs ) ● Long acting ( 24hrs ) P.K Boy’s slides Boy’s slides ● Increase cardiac output (α2 block) ● Decrease peripheral vascular resistance. ● Pharmacologi Postural (orthostatic) hypotension. “Due to baroreceptor reflex, pull of gravity and reduced BP cal actions contribute to low venous return which causes hypotension when standing” ● Reflex tachycardia due to fall in B.P, mediated by baroreceptor reflex and due to block α2 in heart. “Baroreceptors are sensors in the aortic arch that sense blood pressure and relay this information to the brain. When baroreceptors sense sudden drop in BP, reflex tachycardia is stimulated.“ In Pheochromocytoma : Should be given before surgical removal to protect against hypertensive crisis. “pheochromocytoma is a tumor of the adrenal medulla that causes an excessive release of Adrenaline + NA (synthesized in the medulla), resulting in an overstimulation of α1 receptors, resulting in hypertension” Phentolamine: ● Dermal necrosis following extravasation of NA. Indication ● Reversal of local anesthesia. ● Hypertensive crisis following abrupt withdrawal of clonidine or ingestion of tyramine in patients MAO inhibitors. PHEochromocytoma symptoms: Phenoxybenzamine: ● Palpitations Raynaud disease & frostbite ● Headache ● Episodic sweating (diaphoresis) ● Postural hypotension. ● Tachycardia ● Headache ADRs ● Nasal stuffiness or congestion ● Vertigo & drowsiness “ caused by the hypotension” ● Male sexual dysfunction (Inhibits ejaculation) “caused by hypotension” Patients with decreased coronary perfusion, because both drugs can precipitate Contradiction arrhythmias and angina. adrenoceptors = adrenergic receptors Selective α1-receptor Antagonists Drug Prazosin Doxazosin Terazosin M.O.A Selective α1- adrenoceptor antagonist Short half Long half life P.K. life - Vasodilation due to relaxation of arterial and venous smooth muscles. - Fall in arterial pressure. α Pharmacological - Less reflex tachycardia than with non-selective - effects blockers. - First dose may produce an orthostatic (standing position) hypotensive response that can result in syncope and fainting. - Treatment of essential hypertension (prior to any disease) with prostate enlargement.(Hypertrophy) - Urinary obstruction associated with benign prostatic hyperplasia (BPH). - Raynaud's disease (rare disorder of the blood vessels, vasospasm) causes some areas of your body such as your fingers and toes to feel numb and cold in response Uses to cold temperatures or stress. When this happens, blood can't get to the surface of the skin and the affected areas turn white and blue. Remember, α receptors stimulate the following: - Vasoconstriction of skin and peripheral blood vessels. - Relaxation of muscles in urinary bladder and contraction of sphincter (urinary retention). And therefore the antagonist drugs will stimulate the opposite effects. 1) Vasodilation 2) Constriction of muscles of bladder and relaxation of urinary sphincter Selective α1A & α2 receptor Antagonists Tamsulosin Yohimbine (Yohim)(bine)(α2) ﺗﻣﯾس وﻟوزﯾن ﯾوھم ﺑﯾن اﺛﻧﯾن (Drug (Uroselective Selective α1A Selective α2 Receptor α1A is present in prostate and Found in —————— neck of bladder. - Relaxation of smooth muscles of Increase nitric oxide “NO” bladder neck & prostate → improve released in the corpus urine flow. cavernosum (male M.O.A - Has minimal effect on blood anatomy) thus producing pressure. Why? It's more selective vasodilator action and on prostate rather than blood contributing to the vessels in the rest of the body. erectile process. Treatment of benign prostatic Used as
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