This presentation contains drugs which blocks the adrenergic system e.g receptor blockers like alpha and beta receptor antagonists, adrenergic neuron blocking agents in details.various animated pictures are also included to make the presentation interesting as well as i have used various diagrams and tables to have better understanding of the topic. Thank you.
introduction ,classification of cholinergic receptor ,and its function ,anti cholinergic agents -atropine and its pharmacology ,semi synthetic and synthetic atropine substitutes
Sympatholytics or Adrenergic AntagonistsAhmad Naeem
Sympatholytics or Adrenergic Antagonists (Introduction, Classification, Alpha Blockers, Beta Blockers Generations, Respirine)
These are drugs which antagonize the receptor action of adrenaline and related drugs.
Mechanism of Action
The adrenergic antagonists (also called adrenergic
blockers or sympatholytics) bind to adrenoceptors but
don’t trigger the usual receptor-mediated intracellular effects.
These drugs act by either reversibly or irreversibly
attaching to the adrenoceptors, thus preventing
activation by endogenous catecholamine's.
Numerous adrenergic antagonists have important
roles in clinical medicine, primarily to treat diseases associated with the cardiovascular system.
α-Adrenergic Blocking Agents
These drugs inhibit adrenergic responses mediated through the α adrenergic receptors without affecting those mediated through β receptors.
Mechanism of action
Drugs that block α adrenoceptors profoundly affect blood pressure. Blockade of these receptors reduces the sympathetic tone of the blood vessels, resulting in decreased peripheral vascular resistance. This induces a reflex tachycardia resulting from the lowered blood pressure.
Non-Selective α adrenergic antagonists
They cause vasodilation by blocking both alpha-1 and alpha-2 receptors. The blockage of alpha-2 receptors will increase the NE release, which will reduce the force of the vasodilation induced by blockade of the alpha-1 receptors. These are useful for patients with pheochromocytoma.
Selective α1 adrenergic antagonists
They cause vasodilation by preventing NE from activating the alpha-1 receptor, resulting in a lowering of the blood pressure, allowing alpha-1 blockers to be used for hypertension. Alpha-1 blockers also cause relaxation of smooth muscle in the prostate, can be useful for the management of benign prostatic hyperplasia (BPH).
Selective α2 adrenergic antagonists
They inhibit negative feedback of NE, stimulating the sympathetic system.
β-Adrenergic Blocking Agents
Mechanism of Action:
These agents blocks the action of substances, such as adrenaline on nerve cells and causes blood vessels to relax and dilate. This allows blood to flow more easily and lowers blood pressure and the heart rate.
Therapeutic Uses:
Beta blockers are used to prevent, treat or improve symptoms in people who have:
Arrhythmia
Heart failure
Chest pain
Heart attacks
Migraine
Certain types of tremors
Adverse Effects:
Asthma
Heart failure
Hypoglycemia
Bradycardia
This presentation contains drugs which blocks the adrenergic system e.g receptor blockers like alpha and beta receptor antagonists, adrenergic neuron blocking agents in details.various animated pictures are also included to make the presentation interesting as well as i have used various diagrams and tables to have better understanding of the topic. Thank you.
introduction ,classification of cholinergic receptor ,and its function ,anti cholinergic agents -atropine and its pharmacology ,semi synthetic and synthetic atropine substitutes
Sympatholytics or Adrenergic AntagonistsAhmad Naeem
Sympatholytics or Adrenergic Antagonists (Introduction, Classification, Alpha Blockers, Beta Blockers Generations, Respirine)
These are drugs which antagonize the receptor action of adrenaline and related drugs.
Mechanism of Action
The adrenergic antagonists (also called adrenergic
blockers or sympatholytics) bind to adrenoceptors but
don’t trigger the usual receptor-mediated intracellular effects.
These drugs act by either reversibly or irreversibly
attaching to the adrenoceptors, thus preventing
activation by endogenous catecholamine's.
Numerous adrenergic antagonists have important
roles in clinical medicine, primarily to treat diseases associated with the cardiovascular system.
α-Adrenergic Blocking Agents
These drugs inhibit adrenergic responses mediated through the α adrenergic receptors without affecting those mediated through β receptors.
Mechanism of action
Drugs that block α adrenoceptors profoundly affect blood pressure. Blockade of these receptors reduces the sympathetic tone of the blood vessels, resulting in decreased peripheral vascular resistance. This induces a reflex tachycardia resulting from the lowered blood pressure.
Non-Selective α adrenergic antagonists
They cause vasodilation by blocking both alpha-1 and alpha-2 receptors. The blockage of alpha-2 receptors will increase the NE release, which will reduce the force of the vasodilation induced by blockade of the alpha-1 receptors. These are useful for patients with pheochromocytoma.
Selective α1 adrenergic antagonists
They cause vasodilation by preventing NE from activating the alpha-1 receptor, resulting in a lowering of the blood pressure, allowing alpha-1 blockers to be used for hypertension. Alpha-1 blockers also cause relaxation of smooth muscle in the prostate, can be useful for the management of benign prostatic hyperplasia (BPH).
Selective α2 adrenergic antagonists
They inhibit negative feedback of NE, stimulating the sympathetic system.
β-Adrenergic Blocking Agents
Mechanism of Action:
These agents blocks the action of substances, such as adrenaline on nerve cells and causes blood vessels to relax and dilate. This allows blood to flow more easily and lowers blood pressure and the heart rate.
Therapeutic Uses:
Beta blockers are used to prevent, treat or improve symptoms in people who have:
Arrhythmia
Heart failure
Chest pain
Heart attacks
Migraine
Certain types of tremors
Adverse Effects:
Asthma
Heart failure
Hypoglycemia
Bradycardia
These are the drugs which antagonize the receptor action of adrenaline and related drugs.
These drugs act by blocking a and/or ß-adrenergic receptors.
α-blockers
PRAZOSIN is a competitive antagonist effective in the management of hypertension. Similar drugs with longer half-lives (e.g. doxazosin, terazosin).
β-blockers
Heart - Decrease heart rate, force of contraction and cardiac output.
Blood Pressure - Decrease in blood pressure (blockage).
Respiratory System – bronchoconstriction.
Eye – Beta-blocking agents reduce intraocular pressure, especially in glaucoma. The mechanism usually reported is decreased aqueous humor production.
Metabolic - Increase LDL and decrease HDL.
Uterus - Relaxation of uterus.
Local anaesthetic - Propranolol has some local anaesthetic action
Lecture 3 Facial cosmetic surgery
Maxillofacial Surgery
Dental Students Fifth Year second semester
Al Azhar University Gaza Palestine
Dr. Lama El Banna
https://twitter.com/lama_k_banna
Lecture 1 Facial cosmetic surgery
Maxillofacial Surgery
Dental Students Fifth Year second semester
Al Azhar University Gaza Palestine
Dr. Lama El Banna
https://twitter.com/lama_k_banna
Facial neuropathology Maxillofacial SurgeryLama K Banna
Lecture 4 facial neuropathology
Maxillofacial Surgery
Dental Students Fifth Year second semester
Al Azhar University Gaza Palestine
Dr. Lama El Banna
https://twitter.com/lama_k_banna
Lecture 2 Facial cosmetic surgery
Maxillofacial Surgery
Dental Students Fifth Year second semester
Al Azhar University Gaza Palestine
Dr. Lama El Banna
https://twitter.com/lama_k_banna
Lecture 12 general considerations in treatment of tmdLama K Banna
Maxillofacial Surgery
Dental Students Fifth Year First semester
Lecture Name 12 general considerations in the treatment of TMJ
Al Azhar University Gaza Palestine
Dr. Lama El Banna
Maxillofacial Surgery
Dental Students Fifth Year First semester
Lecture Name TMJ temporomandibular joint
Lecture 10
Al Azhar University Gaza Palestine
Dr. Lama El Banna
https://twitter.com/lama_k_banna
Lecture 11 temporomandibular joint Part 3Lama K Banna
Maxillofacial Surgery
Dental Students Fifth Year First semester
Lecture Name TMJ temporomandibular joint Part 3
Lecture 11
Al Azhar University Gaza Palestine
Dr. Lama El Banna
Maxillofacial Surgery
Dental Students Fifth Year First semester
Lecture Name TMJ anatomy examination 2
Lecture 9
Al Azhar University Gaza Palestine
Dr. Lama El Banna
Lecture 7 correction of dentofacial deformities Part 2Lama K Banna
Maxillofacial Surgery
Dental Students Fifth Year First semester
Lecture Name Correction of dentofacial deformities Part 2
Lecture 7
Al Azhar University Gaza Palestine
Dr. Lama El Banna
Lecture 8 management of patients with orofacial cleftsLama K Banna
Maxillofacial Surgery
Dental Students Fifth Year First semester
Lecture Name management of patients with orofacial clefts
Lecture 8
Al Azhar University Gaza Palestine
Dr. Lama El Banna
Lecture 5 Diagnosis and management of salivary gland disorders Part 2Lama K Banna
Maxillofacial Surgery
Dental Students Fifth Year First semester
Lecture Name Salivary gland 2
Diagnosis and management of salivary gland disorders Part 2
Al Azhar University Gaza Palestine
Dr. Lama El Banna
Lecture 6 correction of dentofacial deformitiesLama K Banna
Maxillofacial Surgery
Dental Students Fifth Year First semester
Lecture Name Correction of dentofacial deformities
Lecture 6
Al Azhar University Gaza Palestine
Dr. Lama El Banna
lecture 4 Diagnosis and management of salivary gland disordersLama K Banna
Maxillofacial Surgery
Dental Students Fifth Year First semester
Lecture Name Salivary gland
Diagnosis and management of salivary gland disorders
Al Azhar University Gaza Palestine
Dr. Lama El Banna
Maxillofacial Surgery 1
Dental Students Fifth Year First semester
Lecture Name maxillofacial trauma Part 3
Al Azhar University Gaza Palestine
Dr. Lama El Banna
Maxillofacial Surgery
Dental Students Fifth Year First semester
Lecture Name maxillofacial trauma part 2
Al Azhar University Gaza Palestine
Dr. Lama El Banna
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
1. ADRENERGIC BLOCKERS
Dr. Mahmoud H. Taleb
Assistant Professor of Pharmacology and Toxicology
Department of Pharmacology and Medical Sciences, Faculty of
Pharmacy- Al azhar University 1
2. Adrenergic blocker
(antagonists/sympatholytics)
Drug that bind to adrenoceptor but do not trigger
the usual receptor-mediated intracellular effect.
Have the opposite effect of adrenergic agents
Also known as adrenergic antagonists or
adrenergic Blocking Agents
Block alpha & beta receptor sites(nonselective)
direct or indirect acting on the release of
norepinephrine and epinephrine.
2
7. A- Non Selective Alpha Blocker
1- Phenoxybenzamine 1 > 2
Irreversible
Covalent binding with receptor
Long duration of action (14 - 48 hrs)
Also blocks 5-HT, ACh & H1 receptors
Inhibits neuronal & extra-neuronal uptake of NE
Absorbed from GIT, low bioavailability
7
8. CVS effect
• Vasodilatation – arteriolar and venous BP
• Magnitude dependent on sympathatic activity at that
time
• postural hypotension
• More marked if hypovolaemia is present
• Baroreceptor reflex activation
• reflex tachycardia
• tends to oppose the fall by HR and CO
Epinephrine reversl: All -adrenergic blockers
reverse -agonist action of epinephrine.
8
9. Other Effects
↓contraction of trigone and sphincterin blood
vessels
urine flow
insulin secretion from islet cells(2 blockers)
Miosis
Nasal stuffiness
adrenergic sweating
9
10. Clinical use:
Phaeochromocytoma
Control of BP
Prior to surgery
Adverse effects:
Postural hypotension
Tachycardia
Nausea & Vomiting
Nasal stuffiness
ejaculation
Contraindication: in patient with decrease
coronary infusion.
10
12. 3- Tolazoline
Similar to phentolamine
Slightly less potent
Better absorption from GIT
Rapidly excreted in urine
Limited clinical application
peripheral vasospastic disease
12
13. B- 1 Selective Agents
Prazosin & Terazosin 1 >>>> 2
Effective in management of hypertension
Low affinity for 2
Relative absence of tachycardia
↓ Triglycerides & LDL, ↑ HDL (favourable)
Both are extensively metabolized by liver
Prazosin shows high 1st Pass effect (50%)
Oral absorption – good
Terazosin :Bioavailability >90%; >18 h action
Uses:
• Hypertension
• BPH
Adverse effects
First dose effect
Postural hypotension
Salt & water retention ( long term use) 13
14. Doxazosin:
Similar to Prazosin but longer t ½ (22 Hr) and
inactive product excreated in feces not in urine.
Alfuzosin :
similar to prazosin
Tamsulosin
Selective α1 anatgonist
Has greater selectivity for α1A subtype
Has greater efficacy for BPH
Relatively smaller effects on blood vessels
14
15. Clinical Uses Of Blockers
Pheochromocytoma
Hypertensive emergencies
Chronic hypertension – non selective blockers are not
used
Peripheral vascular diaease
spastic (Raynauds), not morphological
Local vasoconstrictor excess– phentolamine useful-
local infiltration
Urinary obstruction – BPH-prazosin, terazosin,
tamsulosin
CHF
α2- selective antagonists do not have any recognised
clinical use. 15
16. Adverse effects α1 – blockers
Postural hypotension( less with α1 selective-
vasodilatation is less)
Reflex tachycardia ( less with α1 selective)
Salt and water retention
Nasal stuffiness
Miosis
Failure of ejaculation
16
22. Timolol and Nadolol
Block β1 & β2 adrenoceptor and are more potent
than propranolol.
Nadolol has a very long duration of action.
Timolol reduces the production of aqueous humor
in the eye. It is used topically in the treatment of
chronic open-angle glaucoma and, occasionally, for
systemic treatment of hypertension.
22
23. Symptoms of overdose include:
abdominal irritation
central nervous system depression
coma
extremely slow heartbeat
heart failure
lethargy
low blood pressure
wheezing
23
24. Selective β1 antagonists
Acebutolol, atenolol, betaxolol, bisoprolol, esmolol,
metoprolol, and nebivolol
Drugs that preferentially block the β1 receptors minimize
the unwanted bronchoconstriction (β2 effect) seen with
propranolol use in asthma patients.
Actions:
lower blood pressure in hypertension
and increase exercise tolerance in angina
Therapeutic use:
In hypertensive patients with impaired pulmonary function.
first-line therapy for chronic stable angina
Because these drugs have less effect on peripheral vascular
β2 receptors, coldness of extremities (Raynaud
phenomenon), a common side effect of β-blockers, is less
frequent. 24
26. Antagonists with partial agonist ctivity
Acebutolol and pindolol
Acebutolol (β1-selective antagonist)
pindolol (nonselective β-blocker) are not pure
antagonists.
These drugs also have the ability to weakly stimulate
both β1 and β2 receptors.
Used in hypertensive patient with moderate bradycardia.
26
27. Antagonists of both α and β adrenoceptors
Labetalol and carvedilol
Labetalol and carvedilol are nonselective β-blockers
with concurrent α1-blocking actions that produce
peripheral vasodilation, thereby reducing blood
pressure.
They contrast with the other β-blockers that
produce initial peripheral vasoconstriction, and
these agents are therefore, useful in treating
hypertensive patients for whom increased
peripheral vascular resistance is undesirable.
Carvedilol also decreases lipid peroxidation and
vascular wall thickening, effects that have benefit in
heart failure. 27
28. Therapeutic use in hypertension and heart failure
Adverse effect:
Orthostatic hypotension.
Dizziness.
28
29. Dr. Mahmoud H. Taleb 29
IV. DRUGS AFFECTING NEUROTRANSMITTER
RELEASE OR UPTAKE
A. Reserpine
Reserpine a plant alkaloid, blocks the Mg2+/adenosine triphosphate
dependent transport of biogenic amines, norepinephrine, dopamine,
and serotonin from the cytoplasm into storage vesicles in the
adrenergic nerves of all body tissues. This causes the ultimate
depletion of biogenic amines. Sympathetic function, in general, is
impaired because of decreased release of norepinephrine. The drug
has a slow onset, a long duration of action, and effects that persist
for many days after discontinuation.
30. B. GUANETHIDINE
Guanethidine blocks the release of stored norepinephrine
as well as displaces norepinephrine from storage
vesicles (thus producing a transient increase in blood
pressure). This leads to gradual depletion of
norepinephrine in nerve endings except for those in the
CNS. Guanethidine commonly causes orthostatic
hypotension and interferes with male sexual function.
30