CVS 8 - The sympathetic nervous system and RAAS

Question 1

Where the baroreceptors located?

Answer 1

Carotid sinus + aortic arch

Question 2

What happens if there is an increase in baroreceptor firing?

Answer 2

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

Question 3

What neurotransmitter do all parasympathetic neurones release?

Answer 3

ACh

Question 4

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

Answer 4

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.

Question 5

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

Answer 5

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)

Question 6

How are the adrenorecepors divided?

Answer 6

Alpha - excitatory on smooth muscle cells

Beta - relaxant on smooth muscle cells + stimulatory on heart

Question 7

Where are beta 1 receptors located?

Answer 7

Heart
Muscle
GI tract

Question 8

Where are beta 2 receptors located?

Answer 8

Bronchi
Vasculature
Uterine Smooth Muscle

Question 9

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

Answer 9

Post-synaptic membrane - they mediate VASOCONSTRICTION

Question 10

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

Answer 10

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)

Question 11

Describe the structure of the adrenoreceptors.

Answer 11

Alpha 1 = Gq protein linked (PLC)

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

Question 12

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

Answer 12

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

Question 13

Which adrenoreceptors do noradrenaline and adrenaline act on?

Answer 13

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

Question 14

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

Answer 14

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

Question 15

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

Answer 15

Noradrenaline = increase, increase, increase, decrease 
Adrenaline = increase, decrease, increase, increase 
Isoprenaline = increase, decrease, same, increase

Question 16

What three elements regulate renin release?

Answer 16

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

Question 17

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

Answer 17

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

Question 18

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

Answer 18

G protein coupled receptors (Gi and Gq)

Question 19

What is the rapid pressor response of angiotensin II?

Answer 19

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

Question 20

What is the slow pressor response of angiotensin II?

Answer 20

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

Question 21

Describe the effects of angiotensin II on the heart.

Answer 21

Increased preload and afterload

Increased vascular wall tension

Question 22

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

Answer 22

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

Question 23

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

Answer 23

Reduce the breakdown of bradykinin

Question 24

What effect do angiotensin II type 1 receptor antagonists have?

Answer 24

Selectively blocks the effects of angiotensin II

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

Question 25

What is the effect of aldosterone?

Answer 25

Increase Na+ reabsorption

Increase K+ and H+ secretion

Question 26

What are two main stimuli for aldosterone release?

Answer 26

Angiotensin II

Increased Potassium

Question 27

What are some harmful effects of aldosterone release?

Answer 27

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

Question 28

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

Answer 28

FLUID LOSS (e.g. severe haemorrhage)