β-Adrenergic blocking agents are competitive antagonists that act on β1 and β2 receptors. Nonselective β-blockers act on both receptors, while cardioselective block primarily β1 receptors. β-Blockers lower blood pressure in hypertension by decreasing cardiac output and sympathetic outflow, without causing postural hypotension. They are effective in treating angina, arrhythmias, myocardial infarction, heart failure, hyperthyroidism, glaucoma, and migraines. Propranolol is a nonselective β-blocker that blocks both β1 and β2 receptors. It is effective for hypertension, angina, arrhythmias, migraine prevention, hyperthyroidism, and glaucoma
The term inotropic state is most commonly used in reference to various drugs that affect the strength of contraction of heart muscle (myocardial contractility). However, it can also refer to pathological conditions. For example, enlarged heart muscle (ventricular hypertrophy) can increase inotropic state, whereas dead heart muscle (myocardial infarction) can decrease it.
Antiadrenergic agents inhibit the signals of epinephrine and norepinephrine. They are primarily postsynaptic adrenergic receptor antagonists (alpha and beta adrenergic receptor antagonists, or "blockers"), inhibiting the downstream cellular signaling pathways of adrenergic receptors. However, there are exceptions: clonidine is an adrenergic agonist at the α2 receptor; since this receptor is located presynaptically, agonism at this receptor inhibits the presynaptic release of adrenaline and noradrenaline, preventing postsynaptic adrenergic receptor activation and downstream signaling.
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The term inotropic state is most commonly used in reference to various drugs that affect the strength of contraction of heart muscle (myocardial contractility). However, it can also refer to pathological conditions. For example, enlarged heart muscle (ventricular hypertrophy) can increase inotropic state, whereas dead heart muscle (myocardial infarction) can decrease it.
Antiadrenergic agents inhibit the signals of epinephrine and norepinephrine. They are primarily postsynaptic adrenergic receptor antagonists (alpha and beta adrenergic receptor antagonists, or "blockers"), inhibiting the downstream cellular signaling pathways of adrenergic receptors. However, there are exceptions: clonidine is an adrenergic agonist at the α2 receptor; since this receptor is located presynaptically, agonism at this receptor inhibits the presynaptic release of adrenaline and noradrenaline, preventing postsynaptic adrenergic receptor activation and downstream signaling.
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Letter from the Congress of the United States regarding Anti-Semitism sent June 3rd to MIT President Sally Kornbluth, MIT Corp Chair, Mark Gorenberg
Dear Dr. Kornbluth and Mr. Gorenberg,
The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
harassment and intimidation at the Massachusetts Institute of Technology (MIT). Failing to act decisively to ensure a safe learning environment for all students would be a grave dereliction of your responsibilities as President of MIT and Chair of the MIT Corporation.
This Congress will not stand idly by and allow an environment hostile to Jewish students to persist. The House believes that your institution is in violation of Title VI of the Civil Rights Act, and the inability or
unwillingness to rectify this violation through action requires accountability.
Postsecondary education is a unique opportunity for students to learn and have their ideas and beliefs challenged. However, universities receiving hundreds of millions of federal funds annually have denied
students that opportunity and have been hijacked to become venues for the promotion of terrorism, antisemitic harassment and intimidation, unlawful encampments, and in some cases, assaults and riots.
The House of Representatives will not countenance the use of federal funds to indoctrinate students into hateful, antisemitic, anti-American supporters of terrorism. Investigations into campus antisemitism by the Committee on Education and the Workforce and the Committee on Ways and Means have been expanded into a Congress-wide probe across all relevant jurisdictions to address this national crisis. The undersigned Committees will conduct oversight into the use of federal funds at MIT and its learning environment under authorities granted to each Committee.
• The Committee on Education and the Workforce has been investigating your institution since December 7, 2023. The Committee has broad jurisdiction over postsecondary education, including its compliance with Title VI of the Civil Rights Act, campus safety concerns over disruptions to the learning environment, and the awarding of federal student aid under the Higher Education Act.
• The Committee on Oversight and Accountability is investigating the sources of funding and other support flowing to groups espousing pro-Hamas propaganda and engaged in antisemitic harassment and intimidation of students. The Committee on Oversight and Accountability is the principal oversight committee of the US House of Representatives and has broad authority to investigate “any matter” at “any time” under House Rule X.
• The Committee on Ways and Means has been investigating several universities since November 15, 2023, when the Committee held a hearing entitled From Ivory Towers to Dark Corners: Investigating the Nexus Between Antisemitism, Tax-Exempt Universities, and Terror Financing. The Committee followed the hearing with letters to those institutions on January 10, 202
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This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
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Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
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2024.06.01 Introducing a competency framework for languag learning materials ...Sandy Millin
http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
Home assignment II on Spectroscopy 2024 Answers.pdf
Autonomic nervous system lecture 8
1. ββ-Adrenergic Blocking Agents-Adrenergic Blocking Agents
All the clinically availableAll the clinically available ββ -blockers are-blockers are
competitive antagonistscompetitive antagonists..
NonselectiveNonselective ββ-blockers act at both-blockers act at both ββ11 andand ββ22
receptors, whereasreceptors, whereas cardioselectivecardioselective ββ
antagonists primarilyantagonists primarily blockblock ββ 11 receptors.receptors.
[Note:There are[Note:There are no clinically usefulno clinically useful ββ22 antagonistsantagonists]]
Although allAlthough all ββ -blockers lower blood pressure-blockers lower blood pressure
in hypertension,in hypertension, they do not induce posturalthey do not induce postural
hypotension, because thehypotension, because the αα-adrenoceptors-adrenoceptors
remain functional.remain functional.
2. Therefore,Therefore, normal sympathetic controlnormal sympathetic control of theof the
vasculature is maintainedvasculature is maintained..
ββ -Blockers are also effective-Blockers are also effective in treating:in treating:
angina,angina,
cardiac arrhythmias,cardiac arrhythmias,
myocardial infarction,myocardial infarction,
congestive heart failure,congestive heart failure,
hyperthyroidism,hyperthyroidism,
and glaucoma,and glaucoma,
as well as serving in theas well as serving in the prophylaxis of migraineprophylaxis of migraine
headaches.headaches.
3. A. Propranolol(Inderal)A. Propranolol(Inderal)
AA nonselectivenonselective ββ antagonistantagonist
Propranolol :Propranolol : is theis the ββ-adrenergic-adrenergic
antagonistantagonist and blocks bothand blocks both ββ11 andand ββ22
receptors.receptors.
Sustained-release preparationsSustained-release preparations forfor
once-a-day dosing are available.once-a-day dosing are available.
4. • Actions:Actions:
• Cardiovascular:Cardiovascular:
• PropranololPropranolol diminishesdiminishes cardiac output,cardiac output,
having bothhaving both negative inotropic andnegative inotropic and
chronotropic effects.chronotropic effects. The resultingThe resulting
bradycardia .bradycardia .
• Cardiac output, work, and oxygenCardiac output, work, and oxygen
consumptionconsumption areare decreaseddecreased by blockade ofby blockade of ββ11
receptors;receptors; these effects arethese effects are useful in theuseful in the
treatment of angina .treatment of angina .
5. • Peripheral vasoconstriction:Peripheral vasoconstriction:
– TheThe reduction in cardiac outputreduction in cardiac output leads toleads to
decreased blood pressure.decreased blood pressure.
• ThisThis hypotensionhypotension triggerstriggers
a reflex peripherala reflex peripheral
vasoconstrictionvasoconstriction that is reflected inthat is reflected in
reduced blood flow to the periphery.reduced blood flow to the periphery.
• On balance, there is a gradualOn balance, there is a gradual reductionreduction
of both systolic and diastolicof both systolic and diastolic bloodblood
pressurespressures in hypertensive patients.in hypertensive patients.
6. No postural hypotension occursNo postural hypotension occurs,,
because thebecause the αα11-adrenergic receptors-adrenergic receptors
that control vascular resistancethat control vascular resistance areare
unaffected.unaffected.
7. • Bronchoconstriction:Bronchoconstriction:
• BlockingBlocking ββ 22 receptorsreceptors inin
the lungs of susceptiblethe lungs of susceptible
patients causespatients causes contractioncontraction
of the bronchiolar smooth muscleof the bronchiolar smooth muscle ..
• This can precipitate a respiratory crisis inThis can precipitate a respiratory crisis in
patients withpatients with chronic obstructivechronic obstructive
pulmonary disease (COPD) or asthma.pulmonary disease (COPD) or asthma.
• are thusare thus contraindicated in patients withcontraindicated in patients with
COPD or asthma.COPD or asthma.
8. • Increased NaIncreased Na++
retentionretention::
• Reduced blood pressureReduced blood pressure causescauses a decrease ina decrease in
renal perfusionrenal perfusion, resulting in an, resulting in an increase in Naincrease in Na++
retention and plasma volume .retention and plasma volume .
• In some cases, this compensatory responseIn some cases, this compensatory response
tends totends to elevate the blood pressureelevate the blood pressure..
• For these patients,For these patients, ββ -blockers are often-blockers are often
combined with acombined with a diuretic to prevent Nadiuretic to prevent Na++
retention.retention.
• By inhibitingBy inhibiting ββ receptors,receptors, renin productionrenin production isis
also preventedalso prevented,, contributing to Nacontributing to Na++
retention.retention.
9. • Disturbances in glucose metabolism:Disturbances in glucose metabolism:
• ββ-blockade leads to :-blockade leads to :
• 1-1-decreaseddecreased glycogenolysisglycogenolysis andand decreaseddecreased
glucagon secretion.glucagon secretion.
• Therefore, if a Type I (insulin-dependent)Therefore, if a Type I (insulin-dependent)
diabeticdiabetic is to be given propranololis to be given propranolol,, veryvery
careful monitoring of blood glucosecareful monitoring of blood glucose isis
essential,essential, because hypoglycemia may occurbecause hypoglycemia may occur
after insulin injection.after insulin injection.
2-2- ββ -Blockers also-Blockers also attenuateattenuate thethe normalnormal
physiologic response to hypoglycemia.physiologic response to hypoglycemia.
10. • Therapeutic effects:Therapeutic effects:
1- In Hypertension:1- In Hypertension:
PropranololPropranolol doesdoes not reduce blood pressurenot reduce blood pressure
in people with normal blood pressure.in people with normal blood pressure.
Propranolol lowers blood pressurePropranolol lowers blood pressure inin
hypertension patients by several differenthypertension patients by several different
mechanisms of action:mechanisms of action:
1.1.Decreased cardiac outputDecreased cardiac output is the primaryis the primary
mechanism.mechanism.
2. decreased sympathetic2. decreased sympathetic outflow from theoutflow from the
CNS .CNS .
11. 2- Glaucoma:2- Glaucoma:
•ββ-Blockers, topically applied-Blockers, topically applied Timolol,Timolol,
•are effective in diminishing intraocularare effective in diminishing intraocular
pressure in glaucoma.pressure in glaucoma.
•This occurs byThis occurs by decreasing the secretiondecreasing the secretion
of aqueous humorof aqueous humor by theby the ciliary body.ciliary body.
•Many patients with glaucoma have beenMany patients with glaucoma have been
maintained with these drugs for years.maintained with these drugs for years.
12. • TheyThey neitherneither affect theaffect the ability of the eyeability of the eye
to focus for near visionto focus for near vision
• nornor changechange pupil size,pupil size, as do theas do the
cholinergic drugs.cholinergic drugs.
• However, in anHowever, in an acute attack ofacute attack of
glaucoma,glaucoma, pilocarpinepilocarpine is still the drug ofis still the drug of
choice.choice.
• TheThe ββ -blockers are only used to treat this-blockers are only used to treat this
disease chronically.disease chronically.
13. 3-Migraine:3-Migraine:
•Propranolol is also effective inPropranolol is also effective in reducingreducing
migrainemigraine when used prophylactically.when used prophylactically.
•ββ-Blockers are valuable in the treatment-Blockers are valuable in the treatment
ofof chronic migraine,chronic migraine, in which theyin which they
decrease thedecrease the incidence and severity ofincidence and severity of
the attacks.the attacks.
14. 4- Hyperthyroidism:4- Hyperthyroidism:
• Propranolol and otherPropranolol and other ββ -blockers are-blockers are
effective ineffective in blunting the widespreadblunting the widespread
sympathetic stimulation that occurs insympathetic stimulation that occurs in
hyperthyroidism.hyperthyroidism.
•In acute hyperthyroidism,In acute hyperthyroidism, ββ -blockers-blockers
may bemay be lifesavinglifesaving in protecting againstin protecting against
serious cardiac arrhythmias.serious cardiac arrhythmias.
15. 5- Angina pectoris:5- Angina pectoris:
•PropranololPropranolol decreases the oxygendecreases the oxygen
requirement of heart musclerequirement of heart muscle and,and,
therefore, is effective in reducing thetherefore, is effective in reducing the
chest pain on exertionchest pain on exertion that is common inthat is common in
angina.angina.
• PropranololPropranolol is therefore useful in theis therefore useful in the
chronic management ofchronic management of stable angina,stable angina,
but notbut not for acute treatment.for acute treatment.
16. 6- Myocardial infarction:6- Myocardial infarction:
•Propranolol and otherPropranolol and other ββ -blockers-blockers have ahave a
protectiveprotective effect on theeffect on the myocardium.myocardium.
•Thus, patients who haveThus, patients who have one myocardialone myocardial
infarction appear to beinfarction appear to be protected against aprotected against a
second heart attacksecond heart attack by prophylactic use ofby prophylactic use of ββ--
blockers.blockers.
•In addition, administration of aIn addition, administration of a ββ-blocker-blocker
immediately following aimmediately following a myocardialmyocardial
infarctioninfarction reducesreduces infarct size and hastensinfarct size and hastens
recovery.recovery.
17. • Propranolol alsoPropranolol also reduces thereduces the
incidence of sudden arrhythmicincidence of sudden arrhythmic deathdeath
after myocardial infarction.after myocardial infarction.
18. • Adverse effects:Adverse effects:
1-1- Bronchoconstriction:Bronchoconstriction:
Propranolol has aPropranolol has a seriousserious andand potentiallypotentially
lethal sidelethal side effect when administered toeffect when administered to anan
asthmaticasthmatic ..
•Deaths by asphyxiationDeaths by asphyxiation for asthmaticsfor asthmatics
administered the drug.administered the drug.
•Therefore, propranolol must never be used inTherefore, propranolol must never be used in
treating any individual with COPD or asthma.treating any individual with COPD or asthma.
19. 2- Arrhythmias:2- Arrhythmias:
•Treatment withTreatment with ββ-blockers must-blockers must
never benever be stopped quicklystopped quickly becausebecause
of the risk of precipitatingof the risk of precipitating cardiaccardiac
arrhythmiasarrhythmias, which may be severe., which may be severe.
•TheThe ββ-blockers must-blockers must be tapered offbe tapered off
gradually for 1 week.gradually for 1 week.
•Long-term treatment with aLong-term treatment with a ββ antagonist leadsantagonist leads
toto up-regulation of theup-regulation of the ββ-receptor-receptor..
•On stop of therapy, the increased receptorsOn stop of therapy, the increased receptors
can worsen angina or hypertension.can worsen angina or hypertension.
20. 3- Disturbances in metabolism:3- Disturbances in metabolism:
• ββ -Blockade leads to decreased-Blockade leads to decreased
glycogenolysis and decreased glucagonglycogenolysis and decreased glucagon
secretion.secretion. Fasting hypoglycemia mayFasting hypoglycemia may
occur.occur.
21. 4- Drug interactions:4- Drug interactions:
•Drugs thatDrugs that interfere with the metabolisminterfere with the metabolism ofof
propranolol, such as cimetidine, fluoxetinepropranolol, such as cimetidine, fluoxetine
(inhibit(inhibit metabolismmetabolism), may), may potentiate itspotentiate its
antihypertensive effects.antihypertensive effects.
• Conversely, those thatConversely, those that stimulate itsstimulate its
metabolism,metabolism, such as barbiturates, phenytoin,such as barbiturates, phenytoin,
and rifampin,and rifampin, can decrease its effectscan decrease its effects..
22. B- Timolol and Nadolol:B- Timolol and Nadolol:
NonselectiveNonselective ββ antagonistsantagonists
Timolol and Nadolol also blockTimolol and Nadolol also block ββ11- and- and ββ22--
adrenoceptors and are moreadrenoceptors and are more potent thanpotent than
propranolol.propranolol.
Nadolol has a very long duration of actionNadolol has a very long duration of action ..
Timolol reducesTimolol reduces the production of aqueousthe production of aqueous
humor in the eye. It is usedhumor in the eye. It is used topicallytopically in thein the
treatment oftreatment of chronic open-angle glaucomachronic open-angle glaucoma and,and,
occasionally, foroccasionally, for systemicsystemic treatment oftreatment of
hypertension.hypertension.
23. C-C- Acebutolol, Atenolol, and Esmolol:Acebutolol, Atenolol, and Esmolol:
SelectiveSelective ββ11 antagonistsantagonists
Drugs that block theDrugs that block the ββ11 receptorsreceptors have beenhave been
developed to eliminatedeveloped to eliminate the unwantedthe unwanted
bronchoconstrictor effect (bronchoconstrictor effect (ββ 22 effect)effect) ofof
propranolol seen amongpropranolol seen among asthmatic patients.asthmatic patients.
This cardioselectivity is thus most at lowThis cardioselectivity is thus most at low
doses and is lost at high doses.doses and is lost at high doses.
24. • Therapeutic use in hypertension:Therapeutic use in hypertension:
• TheThe cardioselectivecardioselective ββ -blockers are useful in-blockers are useful in
hypertensive patients withhypertensive patients with impairedimpaired
pulmonary function.pulmonary function.
• Because these drugs haveBecause these drugs have less effect onless effect on
peripheral vascularperipheral vascular ββ22 receptorsreceptors, the, the coldnesscoldness
of extremitiesof extremities (a common side effect of(a common side effect of ββ
-blocker therapy)-blocker therapy) is less frequent.is less frequent.
• CardioselectiveCardioselective ββ -blockers are useful in-blockers are useful in
diabetic hypertensivediabetic hypertensive patients who arepatients who are
receivingreceiving insulin or oral hypoglycemic agents.insulin or oral hypoglycemic agents.
25. Pindolol and Acebutolol:Pindolol and Acebutolol:
(Antagonists with partial agonist(Antagonists with partial agonist
activity)activity) Actions:Actions:
• Cardiovascular:Cardiovascular: areare not pure antagonistsnot pure antagonists;;
they have thethey have the ability to weakly stimulate bothability to weakly stimulate both
ββ11 andand ββ22 receptors and are said to havereceptors and are said to have
intrinsic sympathomimetic activity (ISA).intrinsic sympathomimetic activity (ISA).
• These partial agonistsThese partial agonists stimulate thestimulate the ββ
receptor to which they are bound,receptor to which they are bound, yet theyyet they
inhibit stimulationinhibit stimulation by the more potentby the more potent
endogenous catecholamines, epinephrine andendogenous catecholamines, epinephrine and
26.
27. • Decreased metabolic effects:Decreased metabolic effects:
• Blockers withBlockers with ISAISA minimize theminimize the
disturbancesdisturbances of lipid and carbohydrateof lipid and carbohydrate
metabolism that are seen with othermetabolism that are seen with other ββ
-blockers.-blockers.
28. • Therapeutic use in hypertension:Therapeutic use in hypertension:
• ββ -Blockers with ISA-Blockers with ISA are effective in hypertensiveare effective in hypertensive
patientspatients withwith moderate bradycardia,moderate bradycardia,
• because abecause a furtherfurther decrease in heartdecrease in heart raterate isis
less pronounced with these drugs.less pronounced with these drugs.
• Carbohydrate metabolismCarbohydrate metabolism isis less affectedless affected
with Acebutolol and pindololwith Acebutolol and pindolol than it is withthan it is with
propranolol, making them valuable in thepropranolol, making them valuable in the
treatment of diabetics.treatment of diabetics.
29. Drugs Affecting NeurotransmitterDrugs Affecting Neurotransmitter
Release or UptakeRelease or Uptake
amphetamine and tyramine,amphetamine and tyramine, they exert theirthey exert their
effectseffects indirectly on the adrenergic neuronindirectly on the adrenergic neuron byby
causing thecausing the release of neurotransmitter fromrelease of neurotransmitter from
storage vesicles.storage vesicles.
Similarly, some agents act on theSimilarly, some agents act on the adrenergicadrenergic
neuron :neuron :
either to interfere witheither to interfere with neurotransmitter releaseneurotransmitter release
or to alter theor to alter the uptake of the neurotransmitter intouptake of the neurotransmitter into
the adrenergic nerve.the adrenergic nerve.
30. A. ReserpineA. Reserpine
Reserpine a plant alkaloid,Reserpine a plant alkaloid, blocks theblocks the
MgMg2+2+
/adenosine triphosphate/adenosine triphosphate (dependent(dependent
transport of biogenic amines)transport of biogenic amines)
norepinephrine, dopamine, and serotoninnorepinephrine, dopamine, and serotonin
from the cytoplasm intofrom the cytoplasm into storage vesiclesstorage vesicles
in the adrenergic nervesin the adrenergic nerves of all bodyof all body
tissues.tissues.
This causes the ultimate depletion of biogenicThis causes the ultimate depletion of biogenic
amines.amines.
31.
32. Sympathetic functionSympathetic function, in general, is, in general, is impairedimpaired
because of decreased release ofbecause of decreased release of
norepinephrine.norepinephrine.
The drug has aThe drug has a slow onset, a long durationslow onset, a long duration ofof
action, andaction, and effects that persist for many dayseffects that persist for many days
after discontinuation.after discontinuation.
GuanethidineGuanethidine
blocks the releaseblocks the release ofof stored norepinephrinestored norepinephrine asas
well aswell as displacesdisplaces norepinephrine from storagenorepinephrine from storage
vesiclesvesicles (thus producing a transient increase(thus producing a transient increase inin
blood pressure).blood pressure).
33.
This leads to gradual depletion ofThis leads to gradual depletion of
norepinephrine in nerve endings exceptnorepinephrine in nerve endings except
for those in the CNS.for those in the CNS.
Guanethidine commonly causesGuanethidine commonly causes
orthostatic hypotensionorthostatic hypotension ..
Supersensitivity to norepinephrine due toSupersensitivity to norepinephrine due to
depletion of the amine can result indepletion of the amine can result in
hypertensive crisis in patients withhypertensive crisis in patients with
pheochromocytoma.pheochromocytoma.
34. C. CocaineC. Cocaine
Although cocaine inhibits norepinephrineAlthough cocaine inhibits norepinephrine
uptake, it is an adrenergic agonist.uptake, it is an adrenergic agonist.
norepinephrine accumulate in thenorepinephrine accumulate in the
synaptic space ,resulting in enhancementsynaptic space ,resulting in enhancement
of sympathetic activity and potentiationof sympathetic activity and potentiation
the action of epinephrine, norepinephrine.the action of epinephrine, norepinephrine.