Beta-blockers work by blocking beta-adrenergic receptors. They have several clinical applications including treating angina, heart failure, hypertension, tremors, migraines and more. They decrease heart rate, myocardial contraction, renin release and intraocular pressure. Potential adverse effects include bradycardia, hypotension, bronchospasm and fatigue. They must be tapered slowly to avoid rebound effects like angina when discontinued.
This document summarizes adrenergic agonists and antagonists. It describes the synthesis and metabolism of catecholamines like dopamine, norepinephrine, and epinephrine. It also discusses the different adrenergic receptor types (alpha and beta), their locations and functions. Various adrenergic drugs are classified and their mechanisms, effects, uses, and adverse effects outlined, including epinephrine, norepinephrine, dopamine, dobutamine, dopexamine, fenoldopam, phenylephrine, clonidine and others.
Your sympathetic nervous system is best known for its role in responding to dangerous or stressful situations.
In these situations, your sympathetic nervous system activates to speed up your heart rate, deliver more blood to areas of your body that need more oxygen or other responses to help your get out of danger.
Its nerve fibers arise from the thoracic and lumbar regions of the spinal cord.
The autonomic ganglia are the synapses between preganglionic and postganglionic neurons. The postganglionic axons then go to the visceral effectors.
Acetylcholine is a neurotransmitter releases in the preganglionic nerve endings and Noradrenaline at postganglionic nerve endings.
The drugs which mimic the action sympathetic division are called sympathomimetics.
They show similar actions as that of catecholamines.
Sympathomimetic
They act by either by directly interacting with adrenergic receptors (alpha or beta) or stimulation of the adrenergic nerve endings.
This document discusses the physiology and pharmacology of the sympathetic nervous system and its receptors. It begins by describing epinephrine as an important regulator of heart and vascular responses to exercise and stress. It then defines sympathomimetic drugs as those that mimic epinephrine's actions. The document goes on to detail the different alpha and beta receptor subtypes, their locations, and examples of agonists and antagonists. It discusses sympathetic neurotransmission and the mechanisms of drug-induced effects. Overall, the document provides a comprehensive overview of the sympathetic nervous system and its clinical applications.
UNIT 03 Final Adrenergic _ Anti Adrenergic Drugs, Educational Platform.pptxMuhammadAbbasWali
This document provides an overview of adrenergic and anti-adrenergic drugs. It begins by outlining the objectives of understanding the effects of stimulating alpha and beta-adrenergic receptors. It then discusses the autonomic nervous system and its sympathetic and parasympathetic divisions. The document focuses on the different types of adrenoceptors (alpha1, alpha2, beta1, beta2, beta3), their sites of action, and effects of stimulation. Examples of agonist and antagonist drugs are provided for each receptor type. The mechanisms and therapeutic uses of norepinephrine, epinephrine, and other adrenergic drugs are also summarized.
This document discusses noradrenergic transmission and classification of adrenoceptor agonists and antagonists. It describes the effects of agonists on alpha and beta receptors, including their pharmacological actions on the cardiovascular, respiratory, and other body systems. It also summarizes the clinical uses of adrenoceptor agonists and antagonists for conditions like hypertension, heart disease, glaucoma, and others. Drugs that affect neurotransmitter release and uptake like reserpine, guanethidine, and cocaine are also briefly discussed.
Skeletal muscle relaxants work by blocking acetylcholine receptors at the neuromuscular junction, relaxing muscles. There are two main types - depolarizing and non-depolarizing. Succinylcholine is the only depolarizing drug used clinically. It causes initial fasciculations before prolonged muscle relaxation. Non-depolarizing drugs like tubocurarine and vecuronium are competitive antagonists that do not activate acetylcholine receptors, preventing muscle contraction. They have short, intermediate, or long durations of action and differ in side effects and metabolism. Dantrolene works via a different mechanism by preventing calcium release in muscles.
Skeletal muscle relaxants work by blocking acetylcholine receptors at the neuromuscular junction, relaxing muscles. There are two main types - depolarizing and non-depolarizing. Succinylcholine is the only depolarizing drug used clinically. It causes initial fasciculations before prolonged muscle relaxation. Non-depolarizing drugs like tubocurarine and vecuronium are competitive antagonists that bind acetylcholine receptors without activating them, preventing muscle contraction. Their effects can be reversed with acetylcholinesterase inhibitors. Dantrolene acts via a different mechanism by preventing calcium release in muscle cells.
This document discusses the autonomic nervous system and drugs that affect it. It begins by describing the organization of the nervous system and autonomic nervous system. It then discusses exceptions in the sympathetic nervous system related to sweat glands, kidneys, and adrenal glands. The document goes on to classify drugs that can mimic or block neurotransmitters in the autonomic nervous system like acetylcholine and adrenaline. It also discusses indirect-acting drugs and different receptor types like muscarinic, nicotinic, alpha, and beta receptors. The locations and functions of these receptors are explained. Finally, examples of drugs are provided that can act as agonists or antagonists at these different receptor types.
This document summarizes adrenergic agonists and antagonists. It describes the synthesis and metabolism of catecholamines like dopamine, norepinephrine, and epinephrine. It also discusses the different adrenergic receptor types (alpha and beta), their locations and functions. Various adrenergic drugs are classified and their mechanisms, effects, uses, and adverse effects outlined, including epinephrine, norepinephrine, dopamine, dobutamine, dopexamine, fenoldopam, phenylephrine, clonidine and others.
Your sympathetic nervous system is best known for its role in responding to dangerous or stressful situations.
In these situations, your sympathetic nervous system activates to speed up your heart rate, deliver more blood to areas of your body that need more oxygen or other responses to help your get out of danger.
Its nerve fibers arise from the thoracic and lumbar regions of the spinal cord.
The autonomic ganglia are the synapses between preganglionic and postganglionic neurons. The postganglionic axons then go to the visceral effectors.
Acetylcholine is a neurotransmitter releases in the preganglionic nerve endings and Noradrenaline at postganglionic nerve endings.
The drugs which mimic the action sympathetic division are called sympathomimetics.
They show similar actions as that of catecholamines.
Sympathomimetic
They act by either by directly interacting with adrenergic receptors (alpha or beta) or stimulation of the adrenergic nerve endings.
This document discusses the physiology and pharmacology of the sympathetic nervous system and its receptors. It begins by describing epinephrine as an important regulator of heart and vascular responses to exercise and stress. It then defines sympathomimetic drugs as those that mimic epinephrine's actions. The document goes on to detail the different alpha and beta receptor subtypes, their locations, and examples of agonists and antagonists. It discusses sympathetic neurotransmission and the mechanisms of drug-induced effects. Overall, the document provides a comprehensive overview of the sympathetic nervous system and its clinical applications.
UNIT 03 Final Adrenergic _ Anti Adrenergic Drugs, Educational Platform.pptxMuhammadAbbasWali
This document provides an overview of adrenergic and anti-adrenergic drugs. It begins by outlining the objectives of understanding the effects of stimulating alpha and beta-adrenergic receptors. It then discusses the autonomic nervous system and its sympathetic and parasympathetic divisions. The document focuses on the different types of adrenoceptors (alpha1, alpha2, beta1, beta2, beta3), their sites of action, and effects of stimulation. Examples of agonist and antagonist drugs are provided for each receptor type. The mechanisms and therapeutic uses of norepinephrine, epinephrine, and other adrenergic drugs are also summarized.
This document discusses noradrenergic transmission and classification of adrenoceptor agonists and antagonists. It describes the effects of agonists on alpha and beta receptors, including their pharmacological actions on the cardiovascular, respiratory, and other body systems. It also summarizes the clinical uses of adrenoceptor agonists and antagonists for conditions like hypertension, heart disease, glaucoma, and others. Drugs that affect neurotransmitter release and uptake like reserpine, guanethidine, and cocaine are also briefly discussed.
Skeletal muscle relaxants work by blocking acetylcholine receptors at the neuromuscular junction, relaxing muscles. There are two main types - depolarizing and non-depolarizing. Succinylcholine is the only depolarizing drug used clinically. It causes initial fasciculations before prolonged muscle relaxation. Non-depolarizing drugs like tubocurarine and vecuronium are competitive antagonists that do not activate acetylcholine receptors, preventing muscle contraction. They have short, intermediate, or long durations of action and differ in side effects and metabolism. Dantrolene works via a different mechanism by preventing calcium release in muscles.
Skeletal muscle relaxants work by blocking acetylcholine receptors at the neuromuscular junction, relaxing muscles. There are two main types - depolarizing and non-depolarizing. Succinylcholine is the only depolarizing drug used clinically. It causes initial fasciculations before prolonged muscle relaxation. Non-depolarizing drugs like tubocurarine and vecuronium are competitive antagonists that bind acetylcholine receptors without activating them, preventing muscle contraction. Their effects can be reversed with acetylcholinesterase inhibitors. Dantrolene acts via a different mechanism by preventing calcium release in muscle cells.
This document discusses the autonomic nervous system and drugs that affect it. It begins by describing the organization of the nervous system and autonomic nervous system. It then discusses exceptions in the sympathetic nervous system related to sweat glands, kidneys, and adrenal glands. The document goes on to classify drugs that can mimic or block neurotransmitters in the autonomic nervous system like acetylcholine and adrenaline. It also discusses indirect-acting drugs and different receptor types like muscarinic, nicotinic, alpha, and beta receptors. The locations and functions of these receptors are explained. Finally, examples of drugs are provided that can act as agonists or antagonists at these different receptor types.
The document discusses the adrenergic system and sympathetic responses. It describes the synthesis, storage, release and uptake of catecholamines like adrenaline. Catecholamines are synthesized from phenylalanine and tyrosine in the liver and stored in vesicles in nerve endings. They are released by nerve impulses and recaptured via neuronal and vesicular uptake pumps. Catecholamines act on alpha and beta adrenergic receptors and are metabolized by monoamine oxidase and catechol-O-methyltransferase. Examples of adrenergic drugs and their uses are also provided.
This document discusses the autonomic nervous system. It begins by defining the somatic and autonomic nervous systems, and their components. It then compares the somatic and autonomic nervous systems. The functions of the sympathetic and parasympathetic nervous systems are described. Cholinergic and adrenergic receptors are explained. The document concludes by discussing cholinergic and adrenergic drugs, including their classifications, mechanisms of action, uses and side effects.
This document discusses the autonomic nervous system. It begins by defining the sympathetic and parasympathetic nervous systems, their functions, and the types of receptors they act on. It then covers cholinergic and adrenergic neurotransmission in more detail. The rest of the document discusses cholinergic and adrenergic drugs, including cholinomimetics, anticholinesterases, antimuscarinics, adrenomimetics, and adrenoceptor antagonists. Key therapeutic uses and side effects of various drugs are provided as examples.
The document discusses adrenergic drugs and their mechanisms and uses. It describes how the sympathetic nervous system activates the fight or flight response through neurotransmitters like epinephrine and norepinephrine. It then covers different classes of adrenergic drugs including sympathomimetics that mimic sympathetic stimulation, vasopressors that constrict blood vessels, bronchodilators for asthma, and anorectics formerly used for weight loss. Specific drugs discussed include epinephrine, dopamine, dobutamine, ephedrine, amphetamines, and selective beta-2 agonists. A variety of conditions treated and contraindications are provided.
Adrenergic agonist agents can be categorized as catecholamines or non-catecholamines. Catecholamines like epinephrine and norepinephrine cannot be used orally due to their short half-life and inability to cross the blood-brain barrier, while non-catecholamines like ephedrine can be used orally and cross the BBB due to their longer half-life. These agents act on alpha and beta adrenergic receptors and are used clinically as pressor agents, cardiac stimulants, bronchodilators, and more. Common adverse effects include anxiety, headache, and arrhythmias.
Adrenergic agonists can be categorized as catecholamines or non-catecholamines. Catecholamines like epinephrine cannot be used orally and have a short half-life, while non-catecholamines like ephedrine can be used orally and have a longer half-life. Examples of adrenergic drugs include pressor agents, cardiac stimulants, bronchodilators, and CNS stimulants. These drugs act through alpha, beta-1, and beta-2 receptors and are metabolized by monoamine oxidase and catechol-O-methyltransferase. Common adrenergic drugs and their uses include epinephrine for anaph
This document discusses the overall actions of adrenaline and noradrenaline on various body systems. It describes how these drugs act on adrenergic receptors to increase heart rate and contractility, increase blood pressure through vasoconstriction and increased peripheral resistance, and cause bronchodilation. The document also outlines the therapeutic uses of adrenergic drugs in conditions like hypotension, asthma, obesity, and uterine relaxation.
About pharmacological classification of sympathetic nervus system both sympathomimetics and sympatholytics drug and all about his pharmacokinetics and pharmacodynamics action on body
The document summarizes the sympathetic nervous system and adrenergic receptors and their ligands. It describes the key neurotransmitter norepinephrine and its receptors (alpha and beta). It then discusses various adrenergic drugs including agonists like epinephrine, norepinephrine, isoproterenol, and antagonists/blockers like phenoxybenzamine, phentolamine, prazosin and their mechanisms and uses.
This document discusses the adrenergic system and adrenergic drugs. It begins by describing the natural and synthetic catecholamines and non-catecholamines. It then discusses the biosynthesis, storage, release, reuptake, and metabolism of catecholamines. The document describes the different types of alpha and beta adrenergic receptors, their molecular effects, locations, and clinical effects. Specific catecholamines like adrenaline, noradrenaline, dopamine, and isoprenaline are discussed in detail regarding their actions, uses, and adverse effects. The therapeutic classifications and uses of various adrenergic drugs are provided.
This document discusses various vasodilators used to treat conditions like hypertension, heart failure, and peripheral vascular disease. It describes different classes of vasodilators including direct-acting vasodilators like calcium channel blockers and drugs that increase cyclic nucleotides, and indirect vasodilators that interfere with the sympathetic nervous system or renin-angiotensin system. Specific vasodilators discussed in detail include nitroglycerin, hydralazine, minoxidil, diazoxide, nitric oxide, and natriuretic peptides. Their mechanisms of action, pharmacological effects, uses, and adverse effect profiles are summarized.
This document discusses drugs that affect the sympathetic nervous system. It begins by describing the autonomic nervous system and sympathetic division. Sympathomimetic drugs mimic the effects of endogenous agonists like epinephrine and norepinephrine. These drugs can directly activate adrenergic receptors or act indirectly. Examples of direct-acting agonists include epinephrine and dopamine. Epinephrine increases heart rate and contractility while constricting some vessels and dilating others. It also has effects in the lungs, kidneys, liver, and adipose tissue. Beta-adrenoceptors are coupled to G proteins to increase cAMP and calcium entry, enhancing contraction. These drugs have therapeutic uses but also side effects like anxiety
This document discusses drugs that act on the autonomic nervous system. It covers neurotransmitters in the somatic and autonomic nervous systems like acetylcholine and catecholamines. It then categorizes and describes drugs that act on the sympathetic and parasympathetic nervous systems, including sympathomimetics, sympathomolytics, parasympathomimetics, and parasympatholytics. Specific drugs are discussed in detail including their mechanisms, uses, doses, and side effects.
Pharmacology of the Autonomic Nervous SystemDiogo Capela
The document discusses the autonomic nervous system and pharmacology of its sympathetic and parasympathetic divisions. It describes the pre- and post-ganglionic fibers, neurotransmitters, and receptors involved. Catecholamines, adrenergic receptors, and drugs that target the sympathetic system like agonists, antagonists, and their effects are summarized. Parasympathetic muscarinic and nicotinic receptors, cholinergic drugs like direct and indirect agonists, and anticholinergic drugs are also outlined.
Unit 3 Drugs Affecting PNS (As per PCI syllabus)Mirza Anwar Baig
This document provides an overview of a lecture on drugs acting on the autonomic nervous system. It discusses the autonomic neurotransmission and classification of drugs into parasympathomimetics, parasympatholytics, sympathomimetics, and sympatholytics. Specific drugs discussed in detail include direct-acting cholinergic agonists like acetylcholine and indirect-acting cholinergic agonists like anticholinesterase agents. Anticholinergic drugs like atropine are also summarized in terms of their mechanisms and therapeutic uses.
This document discusses adrenergic agonists, which are drugs that activate adrenergic receptors stimulated by norepinephrine or epinephrine. It describes the different types of adrenergic receptors (α1, α2, β1, β2, β3) and the effects of activating each receptor type, such as vasoconstriction, cardiac stimulation, vasodilation, and bronchodilation. It then covers specific adrenergic agonists like epinephrine, isoproterenol, dopamine, phenylephrine, terbutaline, and ephedrine, describing their receptor selectivity, therapeutic uses, and potential adverse effects.
This document discusses drugs acting on the gastrointestinal tract, including those used to treat peptic ulcer disease, antiemetics, and laxatives. It outlines various drug classes used for peptic ulcers like H2 receptor antagonists, proton pump inhibitors, and antibiotics for H. pylori. It also describes antiemetic drugs that work on different receptor types to treat nausea and vomiting. Finally, it covers different classes of laxatives like bulk forming, stool softeners, lubricants, osmotic, and stimulant laxatives.
This chapter discusses the basic principles of pharmacokinetics, which describes what the body does to a drug. It covers the four main pharmacokinetic processes - absorption, distribution, metabolism, and elimination - that determine the onset, intensity and duration of a drug's effects. The chapter also briefly outlines common routes of drug administration and factors that influence the pharmacokinetic processes.
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The document discusses the adrenergic system and sympathetic responses. It describes the synthesis, storage, release and uptake of catecholamines like adrenaline. Catecholamines are synthesized from phenylalanine and tyrosine in the liver and stored in vesicles in nerve endings. They are released by nerve impulses and recaptured via neuronal and vesicular uptake pumps. Catecholamines act on alpha and beta adrenergic receptors and are metabolized by monoamine oxidase and catechol-O-methyltransferase. Examples of adrenergic drugs and their uses are also provided.
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3. Table 1: Distribution of adrenoceptor subtypes and
their actions
Type Tissue Actions
Alpha1
Most vascular smooth
muscles
Contraction
Pupillary dilator muscle Mydriasis
Heart Increase force of
contraction
Alpha2 Adrenergic nerve terminals Inhibition of transmitter
release
Platelets Aggregation
Beta1 Heart Increased rate and force of
contraction
Beta2 Respiratory, uterine, and
vascular smooth muscle
Relaxation
Human liver Glycogenolysis
Beta3 Fat cells Lipolysis
4. Site of α1– adrenoceptors & effects of their
stimulation
• In vascular smooth muscle.
– α1 stimulation cause VC :
• Vasoconstriction in the skin & viscera cause increase PVR
causing increase BP
• Vasoconstriction in the nasal blood vessels cause relief
congestion
• In the radial muscle of iris.
– α1 stimulation causes contraction of the radial muscle causing
mydriasis (dilation of the pupil)
• In the smooth muscle of the sphincters of GIT.
– α1 stimulation cause contraction of all sphincters.
– In the smooth muscle of internal sphincter of urinary bladder .
α1a subtypes stimulation cause contraction and closure of the
sphincters (ppt urinary retention)
5. a1 - selective agonists
1. Phenyl Ephrine
• It is relatively selective α1–agonist
• It is directly acting
• PK: not-catecholamine and thus not metabolized by COMT
• It has longer duration of action than other catecholamines
Clinical uses:
• As a mydriatic agent to examine the fundus of the eye
– It acts on α1 – receptors in the radial dilator pupillary muscle
• As a decongestant
– Used as nasal drops to cause VC in the nasal blood vessels & relief
congestion
• As a vasopressor agent in case of hypotension
– α1 stimulation causes VC leading to increase BP
6. a2 - selective agonists
a2 - selective agonists
Activate presynaptic a2 receptors in the cardiovascular control
center in the CNS => reduced sympathetic nervous system
activity => blood pressure decrease
α2 stimulation leads to decrease Norepinephrine release In
adrenergic nerve terminals (presynaptic).
causing
– relaxation of smooth muscle
• In platelets.
– Increase platelets aggregation
Clinical applications:
Hypertension
• Clonidine
• Guanfacine
7. Clonidine
• It is α2 – selective agonist
• However, this is sympatholytic agent,
used in treatment of hypertension
– It acts centrally at presynaptic α2-adrenoceptor.
This leads to decrease in NE release and to
decrease in PVR.
– Note: Although it is adrenergic agonist, clonidine
acts as a central sympatholytic drug.
• Overdose stimulates peripheral postsynaptic α1
adrenoceptors & cause hypertension by
vasoconstriction
8. Clonidine
Use- treatment of systemic hypertension.
– Low dose Clonidine (50-100μg/dl) is used in
migraine prophylaxis
Adverse effects:
• dry mouth
• Sedation, depression
• Sexual dysfunction
• Bradycardia
• Withdrawal syndrome (rebound hypertension)
follows abrupt discontinuation of long-term
therapy with clonidine in some hypertensive
patients. 8
9. Methyldopa
• Centrally acting antihypertensive agent.
• metabolized to α-methylnorepinephrine in the
brain
– activate central α2 receptors and lower blood
pressure in a manner similar to that of clonidine.
• Safe and preferable anti-hypertensive agent
during pregnancy
9
10. Site of β 1 – adrenoceptors & effects of their
stimulation
• In the heart.
– β 1 stimulation causes
• In S.A node : increase HR (+ve chronotropic)
• In Myocardium tissue : increase contractility (+ve
inotropic)
• In Conducting system : increase conduction velocity
(+ve dromotropic)
• In the Juxtaglomerular Apparatus of the kidney.
– β 1 stimulation cause increased renin release. Then causes
increase in BP
11. Site of β 1 – adrenoceptors & effects of their
stimulation
β 1 - selective agonists
Clinical applications:
• Dobutamine: synthetic analogue of dopamine
– Strong inotropic effect with little chronotropic effect =>
increase in cardiac output without significant increase in
heart rate
• Used in certain types of shock (very low blood pressure) and
heart failure(short-term treatment of impaired cardiac
function after cardiac surgery, MI etc.)
12. Site of β 2–adrenoceptor & effects of their stimulation
• In the bronchial smooth muscle (very important clinically).
– β2 stimulation causes relaxation of smooth muscle
(bronchodilatation)
• In the smooth muscle of blood vessels supplying the skeletal
muscle.
– β2 stimulation causes relaxation of smooth muscle
(Vasodilatation)
• In the smooth muscle of GIT wall.
– β2 stimulation cause relaxation of the wall leading to
decreased peristalsis
• In the smooth muscle of the wall of urinary bladder.
– β 2 stimulation causes relaxation of the wall (opposite to
ACH)
13. • In the smooth muscle of the uterus
– β2 stimulation causes relaxation of the uterus
So, β2 agonists
• In the liver.
– β2 stimulation causes increased Glycogenolysis &
Gluconeogenesis
• In the pancreas.
– β2 stimulation causes slight increase in insulin secretion
Then, what is the effect of β2 stimulation on blood sugar?
b2 - selective agonists
Asthma:
• b2 - selective agonists target predominantly the respiratory system
Site of β 2–adrenoceptor & effects of their
stimulation
14. β2 – adrenoceptors…
• In ciliary muscle.
– β2 stimulation causes
relaxation of the ciliary muscle
leading to
• Accommodation for far
vision
• Decrease outflow of
aqueous humor via the
canal of Schlemm
• In the ciliary epithelium
– β2 stimulation causes
increased production of
aqueous humor
Can we use b-adrenergic
agonists for glaucoma?
15. β2 -Selective Drugs
• widely used for the treatment of asthma.
• Short acting : Salbutamol, Metaproterenol,
Terbutaline
– Use- long-term treatment of obstructive airway
diseases, asthma, and for treatment of acute
bronchospasm.
• Long acting: Salmeterol, formeterol
- use -nocturnal asthma.
16. β2 -Selective Drugs
Ritodrine
• It is another β2 – selective agonist
• It is used to delay premature labour
– β 2 stimulation leads to relaxation of uterine
smooth muscle leading to delay of labour.
• This is done to ensure adequate maturation of
fetus
17. Amphetamine
• indirectly acting sympathomimetic
• It is non-selective adrenergic agonist, non-catecholamine
– Acts mainly, indirectly via enhancing NE release and DA.
– blocks its reuptake into the cytoplasm of the nerve terminal.
– has potent peripheral effects on α1, α2 and β1 receptors, but
not β2 receptors.
– Since it is non-catecholamine, it can be given orally
– It is lipid–soluble enough to be absorbed from intestines
and goes to all parts including CNS (This leads to CNS
stimulation like Restlessness and Insomnia).
– t1/2 = 45 – 60 min (long duration of action)
– It is metabolized in the Liver
17
18. Clinical use of Amphetamine-like drugs
• To suppress appetite
– In very obese persons.
• In narcolepsy
– Narcolepsy is irresistible attacks of sleep during the
day in spite of enough sleep at night
Decreased sense of fatigue
Elevation of mood,with increased initiative, self-
confidence
• Ability to concentrate
• Physical performance in athletes is improved
• Attention deficit-hyperactivity disorder /ADHD/
19. Amphetamines
Side effects
• The side effects are due to chronic use
• These include :
– Tolerance
– Dependence
– Addiction
– Psychosis
– Hypertension
20. Side – effects of sympathomimetic drugs:
• On the CVS
– Hypertension
– Cardiac arrhythmia
– Myocardial infarction
– Increased severity of angina pectoris and of myocardial
infarction
• On the eye
– Increased I.O.P leading to Glaucoma
• On the CNS(Restlessness, anxiety)
• Tachycardia (β2)
• Bradycardia(alpha 1)
23. Alpha blockers
I. irreversible blockers
• in their interaction with these receptors;
irreversible drugs do not dissociate.
– Phenoxybenzamine
ii. reversible blockers
• Reversible antagonists dissociate from receptors
a. Non-selective α antagonists
– Phentolamine, Tolazoline and Ergot derivatives
b. Selective α-antagonists
– α1 Selective antagonists:
• prazosin, doxazosin, terazosin, and tamsulosin
– α2 selective antagonists:
• Yohimbine
23
24. Therapeutic Uses of a1 - Adrenergic Receptor Blockers
1/Pheochromocytoma
• a tumor of the adrenal medulla or sympathetic ganglion cells.
• The tumor secretes catecholamines, especially NE and
epinephrine.
• intermittent or sustained hypertension, headaches,
palpitations, and increased sweating.
• useful in the preoperative management of patients with
pheochromocytoma
• The tumor may be surgically removable, and it is essential to
block α- and β-adrenoceptors before surgery is begun to avoid
the effects of a sudden release of catecholamines when the
tumour is disturbed.
• A combination of phenoxybenzamine and atenolol is effective
for this purpose.
25. Therapeutic Uses of a1 - Adrenergic Receptor
Blockers
2/Hypertension
3/ treatment of peripheral vasospastic disease ie
Raynauds disease to improve perfusion
4/ Treatment of local excess concentration of a
vasoconstrictor in order to prevent necrosis.
26. Therapeutic uses of a1 - adrenergic receptor blockers…
5/ Urinary Obstruction: BPH
• common in elderly men: weak
stream, urinary frequency, and
nocturia.
• surgical treatments
• drug therapy : Prazosin,
doxazosin, terazosin
tamsulosin/Alpha1A/
• improving urine flow
• partial reversal of smooth
muscle contraction in the
enlarged prostate and in the
bladder base.
• Prazosin, terazosin and
doxazosin used in the treatment
of BPH
30. Clinical applications of β -Blockers
• Antiangina: Decreases demand for myocardial oxygen
• Cardioprotective: Inhibits stimulation from circulating
catecholamines(pheochromocytoma)
• Class II antiarrhythmics
• Antihypertensive
• Some are used to treat heart failure (early stage to
prevent cardiac remodeling)
C. Glaucoma: (timolol)
• diminish IOP in glaucoma by decreasing the secretion
of aqueous humor by the ciliary body.
d. Hyperthyroidism: blunting the widespread sympathetic
stimulation that occurs in hyperthyroidism
31. Clinical applications…
• -Migraine prophylaxis:
blockade of
catecholamine-induced
vasodilation in the brain
vasculature
• -tremor
• -performance Anxiety
/ stage fright
32. Beta-Blockers - Adverse Effects
• B1 –blockade /cardiac/: -bradycardia; hypotension
• B2 blocked :Bronchocostriction; muscle fatigue
• -PVD
• -decreased blood flow to vital organ
• Metabolic: - Increase hypoglycemic effect of
insulin(IDDM)
NB- can also mask symptoms of hypoglycemia
• Sudden withdrawal : angina pectoris ,sudden
death
- tapering the dose of the B- blocker for several
weeks before discontinuation.