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YR2 LCRS Pharmacology > 9. SNS antagonists > Flashcards

9. SNS antagonists Flashcards

1
Q

list the sympathetic effects on the body

A
  • dilates pupil
  • inhibits salivation
  • relaxes bronchi
  • accelerates heart
  • inhibits digestive activity
  • stimulates glucose release by liver
  • secretion of epinephrine and norepinephrine from kidney
  • relaxes bladder
  • contracts rectum
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2
Q

what is the 𝛼1 SNS receptor involved in?

A

vasoconstriction, relaxation of GIT

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3
Q

what is the 𝛼2 SNS receptor involved in?

A

inhibition of transmitter release, contraction of vascular smooth muscle, CNS actions

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4
Q

what is the 𝛽1 SNS receptor involved in?

A

increased cardiac rate and force of contraction, relaxation of GIT, renin release from kidney

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5
Q

what is the 𝛽2 SNS receptor involved in?

A

bronchodilation, vasodilation, relaxation of visceral smooth muscle, hepatic glycogenolysis

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6
Q

what is the 𝛽3 SNS receptor involved in?

A

lipolysis

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7
Q

where are autoreceptors and what do they do? Give an example of an autoreceptor

A

autoreceptors are found in the presynaptic membrane

they monitor the NT environment within the synapse and influence the synthesis and release of NT from the presynaptic knob

E.g. presynaptic 𝛼2 adrenoreceptors have a negative effect on the synthesis and release of NA from the nerve terminal

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8
Q

describe the selectivity of common adrenoreceptor antagonists

A

carvedilol: non-selective (𝛼1+ Ξ²1 + Ξ²2) - alpha-1 blockade gives additional vasodilator properties
phentolamine: 𝛼1 + 𝛼2 (equal affinity)
propranolol: 𝛽1 + 𝛽2 (equal affinity)
prazosin: 𝛼1
atenolol: 𝛽1 selective
nebivolol: 𝛽1 selective but also potentiates NO
sotalol: 𝛽1 + 𝛽2 but also inhibits K+ channels

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9
Q

what are the main clinical uses of SNS antagonists and false transmitters?

A
  • hypertension
  • cardiac arrhythmias
  • angina
  • glaucoma
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10
Q

what is hypertension defined as?

A

being consistently over 140/90mmHg

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11
Q

what is hypertension a major risk factor for?

A
  • stroke (causes around 50% of ischaemic strokes)
  • heart failure
  • MI
  • chronic kidney disease
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12
Q

what are the main tissue targets for anti-hypertensives?

A
  • heart: sympathetic nerves innervate the heart and increase HR and CO
  • kidneys: sympathetic nerves innervate the kidneys and increase renin production which increases blood volume
  • arterioles: sympathetic nerves cause venoconstriction
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13
Q

where do beta-blockers work?

A

ANTIHYPERTENSIVE

  • heart (𝛽1) to reduce HR and CO (but this effect disappears in chronic treatment)
  • kidney (𝛽1) to reduce renin production, reduce angiotensin II release (which is a potent vasoconstrictor and causes aldosterone release)

common long-term feature is a reduction in peripheral resistance.

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14
Q

how do beta-blockers antagonise beta receptors?

A

presynaptic 𝛽1 receptors increase NA release so blockade causes loss of NA promoting factors

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15
Q

what are the unwanted effects of beta antagonists?

A
  • BRONCHOCONSTRICTION: in patients with asthma/COPD and patients with obstructive lung disease (e.g. bronchitis)
  • CARDIAC FAILURE: in patients with heart disease who rely on a level of sympathetic drive to maintain an adequate CO
  • FATIGUE: due to reduced CO and reduced skeletal muscle perfusion (due to 𝛽2 blockade on vasculature)
  • HYPOGLYCAEMIA: 𝛽-blockers mask the symptoms of hypoglycaemia (sweating, palpitations, tremor) and inhibit glycogen breakdown (block 𝛽2)
  • COLD EXTREMITIES: loss of 𝛽-receptor mediation vasodilation
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16
Q

what is the advantage of atenolol over propranolol?

A

propranolol is a non-selective beta blocker (for 𝛽1 + 𝛽2) whereas atenolol is 𝛽1 selective (cardio-selective) so it antagonises the effects of NA on the heart but has less of an effect on airways so is safe with asthmatic patients

17
Q

what is the advantage of carvedilol over atenolol and propranolol as an anti-hypertensive?

A

carvedilol antagonises both 𝛽1 + 𝛼1 receptors so can impact vasculature and TPR. it works more on 𝛽1 receptors and causes a decrease in HR or CO

18
Q

compare how 𝛼1 and 𝛼2 receptors work

A

both G-protein linked receptors

𝛼1-receptors: Gq- linked (PLC -> increased intracellular calcium), postsynaptic on vascular smooth muscle

𝛼2-receptors: Gi-linked (decreased cAMP -> decreased NA release), presynaptic autoreceptors inhibiting NA release

19
Q

describe the actions of the alpha -blockers prazosin and phentolamine

A

prazosin: 𝛼1 selective blocker which inhibits vasoconstrictor activity of NA
phentolamine: non-selective, used to treat pheochromocytoma-induced hypertension (has GI side effects)

20
Q

what is the general effect of alpha adrenoreceptor blockers?

A
  • fall in TPR
  • fall in BP
  • postural hypotension
  • CO/HR increases (reflex response to fall in arterial pressure) leading to baroreceptor mediated tachycardia
  • blood flow through cutaneous and splanchnic vascular beds increases
21
Q

why is phentolamine no longer in clinical use?

A

phentolamine causes vasodilation and a fall in BP due to blockade of 𝛼1 adrenoceptors however blockade of presynaptic 𝛼2 adrenoceptors removes the inhibitory effect on NA release so there is an increase in NA release. this enhances the reflex tachycardia, increases GIT motility and leads to diarrhoea

22
Q

why do 𝛼2 receptors and baroreceptors reduce the effectiveness of phentolamine?

A

blockade of 𝛼2 receptors -> less negative feedback -> increased NA release -> NA competes with phentolamine for 𝛼1 receptor -> reduced effectiveness

reduced arterial pressure -> reduced baroreceptor firing rate -> increased sympathetic and decreased parasympathetic activity from medulla -> if the overall effect is sympathetic this increases HR and CO

23
Q

why is prazosin a better alpha blocker than phentolamine?

A

prazosin causes vasodilation and a fall in BP but because it is selective for 𝛼1 the 𝛼2 feedback remains intact

it decreases LDLs (decreases bad cholesterol) and increases HDLs (increases good cholesterol)

24
Q

describe the actions of methyldopa

A

methydopa is an anti-hypertensive drug that is a β€˜false transmitter’

it is taken up by noradrenergic neurones and enters the NA synthesis pathway where it is decarboxylated and hydroxylated to form the false transmitter 𝛼-methyl-NA. 𝛼-methyl-NA enters the synapse, has much less of an effect on adrenoceptors and is not deaminated within the neurone by MAO so can accumulate in larger quantities than NA and displace it

25
Q

what effect does 𝛼-methyl-NA have on 𝛼2 receptors?

A

𝛼-methyl-NA is a good 𝛼2 receptor agonist so increases the negative feedback of NA via 𝛼2 and therefore promotes sympathetic inhibition in 2 ways

this results in improved blood flow (less vasoconstriction)

26
Q

what is the effect of 𝛼-methyl-NA on pregnant women?

A

no adverse effects on the foetus despite cross the blood-placenta barrier

27
Q

what are the side effects of methyldopa?

A

dry mouth, sedation, orthostatic hypotension, male sexual dysfunction

28
Q

how may beta-blockers be used to treat arrhythmias?

A

𝛽-adrenoceptor antagonists act on 𝛽1 receptors on the heart to increase the refractory period of the AV node which interferes with AV conduction on atrial tachycardias to slow ventricular rate. this means the arrhythmia is not aggravated from increased sympathetic drive to the heart

29
Q

what is angina?

A

pain caused by poor blood flow through coronary vessels - strongly linked to atherosclerosis

30
Q

what are the different types of angina?

A

STABLE - pain on exertion. increased demand on the heart due to fixed narrowing of the coronary vessels (e.g. atheroma)

UNSTABLE - pain with less and less exertion. platelet-fibrin thrombus associated with a ruptured atheromatous plaque but without complete occlusion of the vessel. risk of infarction.

VARIABLE - occurs at rest. caused by coronary artery spasm. associated with atheromatous disease

31
Q

how may beta-blockers be used to treat angina?

A

at low doses, 𝛽1-selective agents (metoprolol) reduce HR and contractile activity without affecting bronchial smooth muscle. myocardial work would be decreased which decreases oxygen demand while maintaining the same degree of effort (does cause some degree of exercise intolerance)

32
Q

what is glaucoma characterised by and caused by?

A

characterised by an increase in intraocular pressure

caused by poor drainage of the aq. humour

33
Q

describe how poor drainage of aq humour occurs in glaucoma

A

NA acts on 𝛽1-receptors on the ciliary body which are linked to carbonic anhydrase. aq humour is produced by blood vessels in the ciliary body via the action of carbonic anyhdrase and the aq humour flows into the posterior chamber, through the pupil to the anterior chamber and then drains into the trabecular network and into the veins and canal of Schlemm. production and poor drainage causes glaucoma

34
Q

how may beta-blockers be used to treat glaucoma?

A

beta-blockers reduce the effectiveness of carbonic anhydrase therefore less aq humour is produced

YR2 LCRS Pharmacology (32 decks)

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