CVS 8 - The sympathetic nervous system and RAAS Flashcards

1
Q

Where the baroreceptors located?

A

Carotid sinus + aortic arch

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2
Q

What happens if there is an increase in baroreceptor firing?

A

This decrease the discharge of the sympathetic nervous system leading to a decrease in blood pressure and heart rate.

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3
Q

What neurotransmitter do all parasympathetic neurones release?

A

ACh

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4
Q

What is the most common neurotransmitter released at the effector end of a sympathetic neurone and what are some exceptions?

A

Noradrenaline
Exceptions: the adrenal medulla acts as a specialised post-ganglionic neurone as the chromaffin cells produce mainly adrenaline (80%) and noradrenaline. Sympathetic neurons to sweat glands release acetylcholine.

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5
Q

Describe the two methods of uptake of catecholamines from the synaptic cleft and state the two enzymes involved in their breakdown.

A

They are either taken up into the presynaptic neuron that released them or into extraneuronal tissue.
Enzymes = Monoamine Oxidase (MAO) and Catechol-O Methyltransferase (COMT)

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6
Q

How are the adrenorecepors divided?

A

Alpha - excitatory on smooth muscle cells

Beta - relaxant on smooth muscle cells + stimulatory on heart

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7
Q

Where are beta 1 receptors located?

A

Heart
Muscle
GI tract

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8
Q

Where are beta 2 receptors located?

A

Bronchi
Vasculature
Uterine Smooth Muscle

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9
Q

Where are alpha 1 receptors located and what is their main function?

A

Post-synaptic membrane - they mediate VASOCONSTRICTION

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10
Q

Where are alpha 2 receptors located and what is their function?

A

They are located on the presynaptic membrane and are involved in negative feedback.
Some are post-synaptic on smooth muscle cells and cause VASOCONSTRICTION (like alpha 1 cells)

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11
Q

Describe the structure of the adrenoreceptors.

A

Alpha 1 = Gq protein linked (PLC)

Alpha 2 + Beta 1 + Beta 2 = Adenylate Cyclase (G alpha)

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12
Q

How do the effects of cAMP on smooth muscle, platelets and cardiomyocytes vary?

A

Increasing cAMP is:
INHIBITORY = smooth muscle + platelets
STIMULATORY = cardiomyocytes (unique, because increases IC calcium so contractility)

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13
Q

Which adrenoreceptors do noradrenaline and adrenaline act on?

A
Noradrenaline = a1 + a2 + b1
Adrenaline = ALL the adrenoreceptors (so a1 a2 b1 b2)
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14
Q

State two synthetic compounds that can act on the adrenoreceptors and which adrenoreceptors do they act on?

A
Isoprenaline = b1 + b2 (pure beta agonist) 
Phenylephrine = a1
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15
Q

What is the effect of a) noradrenaline, b) adrenaline and c) isoprenaline on systolic BP, diastolic BP, mean BP and heart rate?

A
Noradrenaline = increase, increase, increase, decrease 
Adrenaline = increase, decrease, increase, increase 
Isoprenaline = increase, decrease, same, increase
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16
Q

What three elements regulate renin release?

A

Amount of sodium reaching the macula densa cells
Blood pressure in the pre-glomerular vessels
Sympathetic activity can increase renin release through beta1 receptors

17
Q

Describe ways in which the renin-angiotensin system can be inhibited.

A

ACE inhibitors - prevent conversion of angiotensin I to angiotensin II
Angiotensin II type I receptors (AT1) antagonists - prevent angiotensin II from exerting its effects
Beta blockers - prevent renin release

18
Q

What type of receptor is an Angiotensin II Type 1 (AT1) receptor?

A

G protein coupled receptors (Gi and Gq)

19
Q

What is the rapid pressor response of angiotensin II?

A

Direct vasoconstriction
Enhanced action of peripheral noradrenaline
Increased sympathetic discharge
Release of catecholamines from adrenal medulla

20
Q

What is the slow pressor response of angiotensin II?

A

Happens over weeks or months
Increased sodium reabsorption
Increased release of aldosterone
Altered renal haemodynamics - renal vasoconstriction + enhanced noradrenaline effects in the kidney

21
Q

Describe the effects of angiotensin II on the heart.

A

Increased preload and afterload

Increased vascular wall tension

22
Q

Why don’t ACE inhibitors completely wipe out angiotensin II production?

A

There is another pathway that converts angiotensin I in to angiotensin II.
This reaction is carried out by CHYMASES

23
Q

What is another effect of ACE inhibitors other than reducing angiotensin II?

A

Reduce the breakdown of bradykinin

24
Q

What effect do angiotensin II type 1 receptor antagonists have?

A

Selectively blocks the effects of angiotensin II

It has NO effects on the bradykinin system because ACE is working perfectly fine

25
Q

What is the effect of aldosterone?

A

Increase Na+ reabsorption

Increase K+ and H+ secretion

26
Q

What are two main stimuli for aldosterone release?

A

Angiotensin II

Increased Potassium

27
Q

What are some harmful effects of aldosterone release?

A
Hypertension -------> Heart Failure
Primary Hyperaldosteronism (associated with benign tumours of the adrenal cortex) = HYPERTENSION + no oedema
Secondary Hyperaldosteronism (excessive response of the body in heart failure and liver failure) = Low/Normal blood pressure + SEVERE OEDEMA
28
Q

What is a potent stimulus for the sympatho-adrenal and renin-angiotensin systems?

A

FLUID LOSS (e.g. severe haemorrhage)