Neuroscience 11 - Sympathetic nervous system and renin angiotensin system

Question 1

Where are noradrenaline and adrenaline systhesised in the neurone?

Answer 1

In the terminal varicosity.

Question 2

What are the subdivisions of adrenoreceptors?

Answer 2

2 groups:

1. Excitatory effects on smooth muscle = a-adrenoreceptor-mediated.
2. Relaxant effects on smooth muscle + stimulatory effects on heart = b-adrenoreceptor-mediated.

Question 3

Where are b1, b2 and b3 adrenoreceptors found?

Answer 3

1. B1 = cardiac muscle, smooth muscle in GI.
2. B2 = Bronchial, vascular and uterine smooth muscle.
3. B3 = fat cells, smooth muscle in GI.

Question 4

What are A1 and A2 adrenoreceptors?

Answer 4

1. A1 = Located post-synaptically (on effector cells). Mediating constriction in resistance vessels.
2. A2 = Located presynaptic (nerve terminal membrane). Activation by neurotransmitter causes negative feedback. HOWEVER, some are post-synaptic on vascular smooth muscle.

Question 5

What is the mechanism for A1 adrenoreceptors?

Answer 5

1. Based on G-proteins activating PLC enzyme.
2. Produced IP3, which releases stored calcium in the cell.
3. This causes activation of smooth muscle and platelets.

Question 6

What is the mechanism for A2 and B arenoreceptors?

Answer 6

1. G-protein linked.
2. Activates cAMP.
3. This is a relaxant in smooth muscle and GI. BUT stimulates heart by increasing intracellular Ca2+.

Question 7

Which adrenoreceptors does noradrenaline activate?

Answer 7

A1, A2 and B1.

Question 8

Which adrenoreceptors does adrenaline activate?

Answer 8

A1, A2, B1, B2.

Question 9

Which adrenoreceptors does dopamine activate?

Answer 9

Weak effects on A1 and B1. Has its own receptors.

Question 10

What are two synthetic catecholamines and which adrenoreceptors do they activate?

Answer 10

1, Isoprenaline = B1, B2.

2. Phenylephrine = A1.

Question 11

What is the effect of systolic BP by noradrenaline, adrenaline and isoprenaline?

Answer 11

1. Noradrenaline = Strong increase.
2. Adrenaline = Increase.
3. Isoprenaline = Slight increase.

Question 12

What is the effect of diastolic BP by noradrenaline, adrenaline and isoprenaline?

Answer 12

1. Noradrenaline = Increase.
2. Adrenaline = Slight decrease.
3. Isoprenaline = Decrease.

Question 13

What is the effect of mean BP by noradrenaline, adrenaline and isoprenaline?

Answer 13

1. Noradrenaline = Increase.
2. Adrenaline = Slight increase.
3. Isoprenaline = no change.

Question 14

What is the effect of HR by noradrenaline, adrenaline and isoprenaline?

Answer 14

1. Noradrenaline = Decrease.
2. Adrenaline = Increase.
3. Isoprenaline = Increase.

Question 15

What causes Renin release? (3)

Answer 15

1. Decrease in NaCl.
2. Decrease in BP.
3. B1 receptor activation in kidney by sympathetic nervous system.

Question 16

What are ACE inhibitors?

Answer 16

Prevent the ACE enzyme converting angiotensin I to angiotensin II.

Question 17

What are B1 blockers?

Answer 17

They block B1 receptors in the kidney to prevent Renin released as a result of sympathetic activity.

Question 18

What are AT1 blockers?

Answer 18

Blocks angiotensin II receptors.

Question 19

What are loop diuretics?

Answer 19

They decrease Na+ getting into kidney = activate renin release.

Question 20

What are AT1 receptors?

Answer 20

1. G-protein coupled receptors.
2. Located in blood vessels, brain, adrenal, kidneys and heart.
3. Activation of AT1 = increase BP.

Question 21

What is the Rapid pressor response? (3)

Answer 21

An effect of angiotensin II that occurs in minutes.

1. Direct vasoconstriction.
2. Enhanced action of peripheral NE.
3. Release of catecholamines from adrenal.

Question 22

What is the Slow pressor response?

Answer 22

AN effect of angiotensin II that occurs in days.

1. Direct effect to increase Na+ reabsorption in proximal tubule.
2. Synthesis and release of aldosterone from adrenal cortex.
3. Renal vasoconstriction.

Question 23

What is vascular and cardiac hypertrophy and remodeling?

Answer 23

1. Increased preload and afterload of heart.

2. Increased vascular wall tension.

Question 24

Do ACE inhibitors prevent the conversion of angiotensin I to angiotensin II?

Answer 24

Yes but not completely, some angiotensin I is converted by chymase.

Question 25

What is the effect of ACE inhibitors on Bradykinin?

Answer 25

ACE inhibitors prevent the breakdown of bradykinin and hence increase vasodilation.

Question 26

What are the effects of aldosterone? (2)

Answer 26

1. Increased Na+ retention = H2O retention.

2. Increased K+ excretion = H+ excretion.

Question 27

What causes the synthesis and release of aldosterone? (3)

Answer 27

1. ACTH (minor influence).
2. Angiotensin II.
3. Increased plasma K+ (big effect).

Question 28

What are the main effects of the sympathoadrenal system and the renin-angiotensin system? (5)

Answer 28

1. Increased BP.
2. Increased HR.
3. Increased Na+/H2O retention.
4. Increased coagulation.
5. Increased platelet activation.

Question 29

What happens if you have too much aldosterone? (2)

Answer 29

1. Primary aldosteronism = high BP

2. Secondary aldosteronism = Heart and liver failure, Na+ retention, oedema and low BP.