This document outlines different classes of adrenergic drugs including agonists and antagonists. Adrenergic agonists can be direct-acting, mimicking norepinephrine, or indirect-acting, promoting norepinephrine release. Examples include epinephrine, norepinephrine, dopamine, and isoproterenol. Adrenergic antagonists block receptors and include alpha blockers like prazosin and beta blockers like propranolol. Indirect antiadrenergic agents decrease norepinephrine release through mechanisms like depletion from neurons (reserpine) or inhibition of release (guanadrel).
About pharmacological classification of sympathetic nervus system both sympathomimetics and sympatholytics drug and all about his pharmacokinetics and pharmacodynamics action on body
About pharmacological classification of sympathetic nervus system both sympathomimetics and sympatholytics drug and all about his pharmacokinetics and pharmacodynamics action on body
This presentation contains a brief introduction of Adrenergic and cholinergic systems and their function in our body.
And a brief description of some adrenergic and cholinergic agents along with their mechanism of action along with their respective Structures.
Systemic Pharmacology Of Autonomic Nervous System. Sympathomimetics AgentsAshish Gadage
Dive into the Intriguing World of Sympathomimetics! Unravel the secrets of Systemic Pharmacology in our exploration of the Autonomic Nervous System. Join us on a journey through the dynamic realm of Sympathomimetic Agents, where science meets adrenaline. From their roles in medicine to the intricacies of their impact, this presentation is your gateway to understanding the pharmacological dance within the Autonomic Nervous System. #Pharmacology #AutonomicNervousSystem #Sympathomimetics
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 a brief introduction of Adrenergic and cholinergic systems and their function in our body.
And a brief description of some adrenergic and cholinergic agents along with their mechanism of action along with their respective Structures.
Systemic Pharmacology Of Autonomic Nervous System. Sympathomimetics AgentsAshish Gadage
Dive into the Intriguing World of Sympathomimetics! Unravel the secrets of Systemic Pharmacology in our exploration of the Autonomic Nervous System. Join us on a journey through the dynamic realm of Sympathomimetic Agents, where science meets adrenaline. From their roles in medicine to the intricacies of their impact, this presentation is your gateway to understanding the pharmacological dance within the Autonomic Nervous System. #Pharmacology #AutonomicNervousSystem #Sympathomimetics
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
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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.
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.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
3. 1. Adrenergic Drugs
A. Adrenergic Agonists
Sympathomimetics
• Drugs that bind to and activate adrenoceptors
directly or indirectly.
• Resemble sympathetic nervous stimulation in
their effect
Classification Adrenergic agonists
Based on chemistry:
1. Catecholamines
• Contain a catechol nucleus & an amine group
Includes
• Natural: NE, EP & DA
• Synthetic: Isoproterenol & dobutamine
3
4. • Common properties:
1. Relatively potent
2. Orally inactive
3. A brief duration of action
4. Cannot cross the BBB
2. Noncatecholamines
• No catechol nucleus
• Ephedrine, phenylephrine, amphetamine,
terbutaline,…
• Direct or indirect action
• Common features:
1. Less potent
2. Orally active
3. Longer duration of action
4. CNS active
4
5. Based on mechanism of action:
1. Direct acting
• Mimic noradrenergic transmission by activating
adrenoceptors
2. Indirect acting
a) Promotion of norepinephrine (NE) release
a) Amphetamines
b) Blockade of NE reuptake
• Cocaine and the tricyclic
antidepressants (e.g., imipramine)
c) Inhibition of NE inactivation
• MAOIs & COMTIs
3. Mixed-acting- direct & indirect
• Ephedrine
5
7. Both types of sympathomimetics, direct or
indirect, ultimately cause activation of
adrenoceptors leading to some or all
characteristic effects of the catecholamines.
Cardiovascular Actions
• The SNS plays an important role in regulating
the CV system.
• By interacting with receptors, adrenergic drugs
directly alter:
• The rate & force of contraction of the heart
• Tone of blood vessels
• This can result in compensatory reflexes to
regulate BP, i.e., drugs that cause
vasoconstriction cause reflex slowing of the
heart.
7
8. Direct-Acting Adrenergic Agonists
• Most common
• Mimicking the actions of natural transmitters (NE,
EP, DA).
Alpha1 activation
• Epinephrine, NE, phenylephrine, ephedrine &
dopamine
Therapeutic applications
• Because of its ability to cause alpha1-mediated
vasoconstriction [skin, viscera & mucous
membranes] used:
1. Mydriasis- eye examination & ocular surgery
2. Hemostasis- control superficial bleeding - EP
3. Reduce nasal congestion- phenylephrine
(topically) & ephedrine (PO) 8
9. • Adverse effects
1. HTN
2. Necrosis- extravasation (Rx-phentolamine)
3. Reflex bradycardia
Alpha2 activation
• Eg. Guanabenz, guanfacine, clonidine, tizanidine
• Alpha 2 receptors are found both in the brain and the
periphery
• Alpha2 receptors in the periphery are located
presynaptically
• Their activation inhibits NE release
• Epinephrine, NE, ephedrine
• No therapeutic applications related to activation of
peripheral alpha2 receptors
9
10. Centrally Acting Alpha2 Agonists
• Act within the CNS to reduce the firing of
sympathetic neurons
• Inhibit the firing of sympathetic neurons
• Decrease the release of NE from sympathetic
nerves
• Decrease activation of peripheral adrenergic
receptors
1. Clonidine
• An antihypertensive drug that acts within the CNS
• An alpha2-adrenergic agonist
• Causes selective activation of alpha2 receptors in
the CNS, in brainstem
• Reduces sympathetic outflow to blood vessels and
the heart 10
11. • Pharmacologic effects
• ↓ BP by VD
• But not ↓HR or CO
• Therapeutic uses
• HTN
• Adverse effects
• Hemolytic anemia- Hg/hematocrit/RBC count
• Hepatotoxicity- LFT
• Others- xerostomia, sexual dysfunction, orthostatic
hypotension, and a variety of CNS effects
11
12. 2. Guanabenz and Guanfacine
• Similar action as clonidine
• Activate brainstem alpha2-adrenergic receptors
• Share the major adverse effects of clonidine
3. Methyldopa and Methyldopate
• Methyldopa is an oral antihypertensive agent
Action is identical to clonidine
But it is a prodrug of methyl NE
Lowers BP by acting at sites within the CNS
• Methyldopate is an IV agent
It is nearly identical to methyldopa in structure &
action
12
14. Beta2 activation
• Ephedrine, epinephrine, isoproterenol, and
terbutaline
• Therapeutic applications
1. Asthma-terbutaline [inhalation]
2. Delay of preterm labor [retodrine]
• Adverse effects
• Hyperglycemia- liver & muscle glycogenolysis
• Tremor- enhanced skeletal muscle contraction
Dopamine receptor activation
• Causes dilation of the vasculature of kidneys
• Treatment of shock
• Dopamine
14
15. Non-selective Direct Acting
Adrenergic Agonists
1. Epinephrine [Adrenaline]
• A catecholamine
• Acts on alpha1, alpha2, beta1, beta2
Therapeutic uses
1. To delay absorption of LAs
2. To control superficial bleeding
3. To elevate BP
4. Nasal decongestion
5. Mydriasis
6. To overcome AV block
7. To overcome cardiac arrest
15
16. 8. Promotes BrD- asthma
9. For anaphylactic shock
Pharmacokinetics
• May be administered:
Topically
By injection (IM)
By inhalation
Inactivation
• Enzymatic (MAO, COMT)
• Uptake
Adverse effects
1. Hypertensive crisis- cerebral hemorrhage
2. Dysrhthmias- hyperthyriod pts
3. Angina pectoris- pts with coronary atherosclerosis
4. Necrosis- following extravasation (IV
phentolamine)
5. Hyperglycemia-beta2-mediated liver & muscle
glycogenolysis- diabetic pts 16
17. 2. Norepinephrine
• A catecholamine
• Acts on alpha1, alpha2, beta1
• Similar to EP
• Only differ from EP, does not act on beta2
receptor
• Nearly identical adverse effects to EP
• But not promote hyperglycemia
• Similar drug interaction as EP
• But limited clinical applications
Only for hypotensive states and cardiac arrest
• Given as IV infusion
17
18. 3. Isoproterenol, metaproterenol
(noncatecholamine)
• A catecholamine
• Acts on beta1 and beta2
Therapeutic uses
1. Cardiac disorders- AV block, cardiac arrest &
shock
2. Asthma
3. Bronchospasm- during anesthesia
Adverse effects
1. Tachydysrhythmias
2. Angina pectoris
3. Hyperglycemia
Drug interactions
Similar to EP
Available as isoproterenol HCl [Isuprel]
solution 18
19. 4. Dopamine, fenoldopam (HTN)
• A catecholamine
• It is a unique adrenomimetic drug in that it
exerts its cardiovascular actions by
1. Interacting with beta1 & alpha1
2. Releasing NE from adrenergic neurons
3. Interacting with specific dopamine receptors
Dose-dependent effects
At low therapeutic doses=D1- dilates renal
vasculature
o ↑GFR, & urinary output
o Used to treat renal failure
At moderate therapeutic doses=beta1
At very high doses= alpha1
19
21. 5. Dobutamine
• A catecholamine
• Acts on beta1
Therapeutic use
Heart failure
Adverse effect
Tachycardia
• Similar drug interaction as dopamine
Available as dobutamine HCl solution
21
22. 6. Phenylephrine
• A noncatecholamine
• Acts on alpha1
Uses
1. For nasal congesion-locally
2. Hypotension-injection
3. Mydriasis- as eye drop
4. With local anesthetics
7. Terbutaline, Albuterol; formeterol& salmeterol
(nocturnal asthma)
• A noncatecholamine
• Acts on beta2
Therapeutic uses
1. Asthma
2. Delay of preterm labor
22
23. Adverse effects
• Tremor
• Tachycardia
7. Ephedrine
• A noncatecholamine
• Acts on alpha1, alpha2, beta1, beta2
• Mixed acting drugs
• Limited uses
1. Asthma
2. Shock
3. Nasal decongestion
• Similar adverse effects as EP
Insomnia- CNS active
23
24. 2 Direct-acting Adrenergic
Antagonists
• Either irreversible or reversible (competition)
binding
• Most are more selective vs. agonists
1. Alpha-adrenergic blocking agents
2. Beta-adrenergic blocking agents
24
26. Alpha-adrenergic Antagonists
A. Nonselective alpha blockers
1. Phentolamine- competitive & reversible
2. Phenoxybenzamine- noncompetitive &
irreversible
Clinical uses
1. Pheochromocytoma
2. Necrosis
3. Orthostatic hAdverse effects
4. ypotension- EP but not NE or IV fluids
5. Greater reflex tachycardia vs. selective ones-
beta blockers
6. Nasal congestion
7. Inhibition of ejaculation
8. Aggravate angina pectoris and myocardial 26
27. B. Selective alpha1 blockers
1. Prazocin 4. Silodosin
2. Alfuzosin 5. Terazosin
3. Doxazosin 6. Tamsulosin
• Competitively block alpha1
Therapeutic application
1. Essential HTN- prazosin, terazosin, doxazosin
2. Reversal of toxicity from alpha1 agonists [HTN,
necrosis- phentolamine]
3. Benin prostatic hyperplasia (BPH)-terazosin,
doxaosin, tamsulosin, alfuzosin, silodosin
4. Pheochromocytoma- severe HTN
[Phenoxybenzamine]
5. Raynaud's disease- peripheral vascular disorders
involving vasospasm in toes and fingers. Local
pain & cold
27
28. Beta-adrenergic Antagonists
• Principal differences:
• Receptor specificity
• Pharmacokinetics
• Indications
• Side effects
• Intrinsic sympathomimetic (partial agonist) activity
• Ability to cause vasodilation
28
29. Based on receptor specificity
1. First-generation(nonselective)
Carteolol, nadolol, penbutolol, pindolol,
propranolol, sotalol & timolol
2. Second-generation (cardioselective—β1)
Acebutolol, atenolol, betaxolol, bisoprolol,
esmolol, metoprolol & nebivolol
3. Third-generation beta blockers (Vasodilation)
Carvedilol, labetalol, and nebivolol
Beta1, beta2, alpha1
Cause VD by two mzms:
1. Blocking alpha1 on blood vessels
2. Promoting synthesis and release of NO
29
30. Based on PK
• High lipid solubility
CNS active
E.g., Propranolol, metoprolol
Elimination via liver
• Low lipid solubility
CNS inactive
E.g., nadolol, atenolol
Elimination via kidney
Intrinsic sympathomimetic activity (ISA)
• Ability of certain beta blockers to act as partial
agonists at beta-adrenergic receptors
• E.g., pindolol
• Preferred to use in bradycardia
• Not given to MI
30
31. Indirect-Acting Antiadrenergic
Agents
• Drugs that prevent activation of peripheral
adrenergic receptors, indirectly.
• Two types:
1. Adrenergic neuron-blocking agents
• Drugs that act within the terminals of sympathetic
neurons
• To decrease NE release
2. Centrally acting alpha2 agonists
• Drugs that act within the CNS
• To reduce the outflow of impulses along
sympathetic neurons.
With both groups, the net result is reduced
activation of peripheral adrenergic receptors.
31
32. Adrenergic Neuron-blocking Agents
• Act presynaptically to reduce the release of NE
from sympathetic neurons
1. Prevents storage [Reserpine]
• Rauwolfia alkaloid (Rauwolfia serpentina)
• Causes depletion of NE from postganglionic
sympathetic neurons
• Decrease activation of all forms of adrenoceptors
• Depletes NE in two ways:
1. Displacement of NE from its storage
sites[vesicles]- exposing to MAO
2. Suppression of NE synthesis- by blocking DA
uptake into presynaptic vesicle
3. Also cause depletion of serotonin, catecholamines
in CNS- deep emotional depression
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33. Pharmacological effects
• Peripheral Effects.
• ↓alpha & beta receptors activation
• ↓HR & CO
• Vasodilation
↓ BP
2. Effects on the CNS
• Sedation
• Severe depression
• Therapeutic Uses
• Mild hypertension with diuretics
• Psychotic States- schizophrenia
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34. • Adverse Effects
• Depression
• Cardiovascular Effects- bradycardia, orthostatic
hypotension & nasal congestion
• GI Effects- ↑gastric acid (ulcer formation), cramps &
diarrhea
2. Inhibit NE release [Guanadrel and
Guanethidine]
• Similar action as reserpine
• CNS inactive
• Diarrhea and severe orthostatic hypotension
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