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Flashcards in SNS Antagonists Deck (40)
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Describe the effects of each type of adrenoceptor.
Alpha 1
Alpha 2
Beta 1
Beta 2
Beta 3

Alpha 1
 Vasoconstriction
 GI tract relaxation
Alpha 2
 Inhibition of transmitter release
 Contraction of vascular smooth muscle
 CNS actions
Beta 1
 Heart – increased heart rate + contractility
 Kidneys – increased renin release
 GI tract relaxation
Beta 2
 Bronchodilation
 Vasodilation
 Relaxation of visceral smooth muscle
 Hepatic glycogenolysis
Beta 3
 Lipolysis


State five adrenoceptor antagonists including the receptors that they block.

Labetalol = alpha 1 + beta 1 (more beta 1 (4:1))
Phentolamine = alpha 1 + alpha 2
Prazosin = alpha 1
Propranolol = beta 1 + beta 2
Atenolol = beta 1


State four main clinical uses of SNS antagonists and false transmitters.



State three elements that contribute to hypertension.

Blood volume
Peripheral vascular tone
Cardiac output


What is the main control of blood pressure?

Sympathetic drive to the kidneys via beta 1 receptors
This triggers renin release from the kidneys (leads to an increase in angiotensin II and aldosterone)


What are beta-1 selective blockers called?

Cardioselective Beta-blockers


What effect is responsible for most of the anti-hypertensive effect of beta-blockers?

Beta 1 blockade in the kidneys – this reduces renin release from the kidneys


What effect does beta-1 blockade have on the heart?

Decrease in heart rate
Decrease in cardiac output


How does the effect of beta-blockers on the heart change?

The effect of beta blockade on the heart disappears with chronic treatment as the heart begins to reset itself


What is the effect of presynaptic beta 1 receptors?

They have a positive facilitation effect on the synthesis and release of neurotransmitter


State four conditions in which you would not give a patient a betablocker. Explain each of them.

Asthma – blockade of beta 2 receptors in the lungs can take away the beta 2 mediated bronchodilation, which can be fatal in asthmatics
Cardiac Failure – these patients rely on a certain degree of sympathetic drive to the heart to maintain adequate cardiac output
COPD – same reason as asthma
Diabetes – beta blockade masks the symptoms of hypoglycaemia (e.g. tremors, palpitations, sweating) and beta 2 blockade also inhibits hepatic glycogenolysis


State some other unwanted actions of beta-blockers.

Cold extremities


What effect does propranolol have on heart rate, cardiac output and blood pressure?

It has little effect on these parameters at rest
It decreases all of these parameters when exercising


Why would you still not give a cardioselective beta-blocker to anasthmatic patient?

Selectivity is dependent on concentration


What are the effects of labetalol?

Acts more on beta 1 than alpha 1
It lowers blood pressure by reducing total peripheral resistance and it induces a change in heart rate and cardiac output (beta 1 mediated)


What is the main mediator of total peripheral resistance?

Alpha 1 mediated vasoconstriction


What are the effects of alpha blockade?

Vasodilation causing a fall in TPR and hence a fall in blood pressure
NOTE: blocking the sympathetic drive can cause postural hypotension


What reflex will be triggered by alpha blockade?

It triggers a baroreceptor mediated reflex tachycardia to increase heart rate and cardiac output


State some of the problems with non-selective alpha blockers (e.g. phentolamine).

Alpha 1 blockade will cause vasodilation and a fall in TPR and blood pressure
But the alpha 2 blockade will mean that you take away the negative effect of alpha 2 on the synthesis and release of noradrenaline so more noradrenaline will be released from the nerve terminal
This enhances the reflex tachycardia
Side effects include increased GIT motility and diarrhoea
Phentolamine is no longer used


What are the effects of prazosin?

Highly selective alpha-1 antagonist
Leads to vasodilation and a fall in blood pressure
You get less tachycardia than with non-selective alpha blockers because the negative effect of alpha 2 on noradrenaline release has not been removed
NOTE: postural hypotension is troublesome
Prazosin also increases HDL and decreases LDL so is becoming more popular as an anti-hypertensive


Describe the mechanism of action of methyldopa.

Methyldopa is taken up by noradrenergic neurones and is decarboxylated and hydroxylated for form alpha-methyl noradrenaline
This is not deaminated by MAO so accumulates more than noradrenaline in the synapse
Alpha-methyl noradrenaline displaces NA from the synaptic vesicles
It is less effective than NA on alpha 1 receptors so does not cause as much vasoconstriction
It is more effective than NA on alpha 2 receptors thus reducing noradrenaline release
It also affects the CNS by inhibiting sympathetic outflow


State some other benefits of methyldopa other than its effect as an anti-hypertensive.

It does not have any adverse effects on foetus’ despite crossing the placenta
It maintains renal and CNS blood flow so it is used in patients with renal insufficiency or cerebrovascular disease
Adverse effects: dry mouth, sedation, postural hypotension, male sexual dysfunction
It is RARELY used


What are arrhythmias usually caused by and why?

Myocardial ischaemia – damage to the heart muscle can result in re-entry of impulses that messes up the heart rhythm


What can precipitate or aggravate arrhythmias?

An increase in sympathetic drive to the heart via beta 1 receptors


What part of the heart’s electrical circuit depends heavily on sympathetic activity?

AV conductance depends heavily on sympathetic activity


What effect do beta antagonists have on the refractory period of the AV node? How does this help in dealing with arrhythmia?

Beta-blockers INCREASE the refractory period of the AV node
It can interfere with AV conduction in atrial tachycardias and slow downventricular rate


What class of drugs are beta-blockers?

Class II anti-arrhythmics


What is propranolol particularly effective at treating?

It is particularly successful in arrhythmias that occur during exercise or mental stress


Define angina.

Chest pain that occurs when the oxygen supply to the myocardium is insufficient for its needs


Describe the three different types of angina.

 Pain on exertion due to a FIXED narrowing
 Pain with less and less exertion culminating with pain at rest
 Atheromatous plaque begins to rupture
 Platelet-fibrin thrombus associated with the ruptured plaque without complete occlusion of the vessel
 High risk of infarction
 Occurs at rest
 Caused by coronary artery spasm
 Associated with atheromatous disease