Sympathetic Nervous and RAS 9

Question 1

Where are baroreceptors found?

Answer 1

In the aortic arch and carotid arteries

Question 2

What does increased baroreceptor activity lead to?

Answer 2

This increases parasympathetic activity which decreases the contractility and heart rate so a decrease in blood pressure occurs

Question 3

What do all parasympathetic nerve terminals release?

Answer 3

Acetylcholine

Question 4

What is released at the paraveterbal sympathetic ganglion?

Answer 4

Acetlycholine in cholinergic receptors

Question 5

What is released at the sympathetic effector arm?

Answer 5

Noradrenaline (except in the adrenal medulla where 80% is adrenaline)

Question 6

How is noradrenaline removed from the cleft?

Answer 6

Uptake 1 = Goes back to neurone that released it

Uptake 2 = goes into extraneuronal cells

Question 7

What breaks noradrenaline down?

Answer 7

MAO (Monoamine Oxidase)

COMT (Catechol - O - Methly transferase)

Question 8

What are the types of adrenoreceptors and what happens when they are stimulated?

Answer 8

Alpha - excitatory effects on smooth muscle

Beta - relaxant effects on smooth muscle and stimulatory effects on the heart

Question 9

What are the subdivisions of beta adrenoreceptors and where are they found?

Answer 9

Beta1 = cardiomyocytes and smooth muscle in GI

Beta2 = Vasculature, bronchi, uterine smooth muscle’

Beta3 = Fat cells

Question 10

What are the subdivisions of alpha adrenoreceptors and where are they found?

Answer 10

Alpha1 = located post-synaptically. Important in mediating constriction or resistance vessels

Alpha2 = Located pre-synaptically on nerve terminals and activation by neurotransmitter causes -ve feedback on further neurotransmitter release

Question 11

Describe the coupling of Alpha1 Adrenoreceptors

Answer 11

Couple with G protein which causes activate of Phopsholipase C (PLC) which converts PIP2 to IP3 which causes release of Ca2+ from intracellular stores. This in turn causes muscle contraction.

Question 12

Decribe the coupling of alpha2 and all Beta adrenoreceptors?

Answer 12

Couple with adenylate cylase which converts ATP to cAMP. This is an inhibitor so prevents contraction of smooth muscle and activation of platelets.

in cardiomyocytes, increase cAMP activates the cell like calcium and so causes contraction. this is unique to cardiocyocytes.

Question 13

What does noradrenaline cause cardiovasularly?

Answer 13

Reflex brachcardia

Question 14

What does adrenaline cause cardiovascularly?

Answer 14

Direct increase in heart rate

Question 15

What does isoprenaline cause cardiovascuarly?

Answer 15

More direct increase in HR (no alpha effects peripherally)

Question 16

Describe the biosynthesis of Angiotensin 2

Answer 16

Angiotensinogen converted to ANgiotensin 1 (Renin). Angiotensin 1 converted to Angiotensin 2 (ACE). Angiotensin 2 converted to angiotensin 3 by aminopeptidase.

Question 17

What are the 3 main elements that increase renin release?

Answer 17

• low amount of sodium that reaches the macula densa
• blood pressure decreased
• increased beta receptor activation

Question 18

How can renin release be affected pharmacologically?

Answer 18

• AT2 receptors can be blocked
• ACE inhibitors stop A2 production
• Beta blockers stop production in kidney
• loop diuretics cause an increase in release as less Na+ reaches the macula densa
• NSAIDS cause an increased renin release

Question 19

What does activation of Angiotensin 2 Type 1 (AT1) Receptors do?

Answer 19

Increase the blood pressure via g protein

Question 20

Where at AT1 receptors found?

Answer 20

• blood vessles
• brain
• adrenals
• kidney
• heart

Question 21

What are the effects of AT2?

Answer 21

• Increased peripheral resistance from vasoconstriction due to enhanced peripheral noradrenaline (RAPID RESPONSE)
• Renal function via increased Na reabsorption from synthesis and excertion of aldosterone (slow response)
• Haemodynamic effects include increased preload and afterload as well as wall tension

Question 22

How can you manipulate RAS pharmacologically?

Answer 22

• Renin inhibitors

- ACE inhibitors but there are chymases in the body that still convert this

Question 23

What does blocking ACE also do other than to AT2?

Answer 23

Stops inactivation of bradykinin (vasodilator)

Question 24

What doe Angiotensin 2 type 1 receptor antagonists do/cause?

Answer 24

• block pressor effects
• stimulation of noradrenline
• secretion of aldosterone
• effects on renal vasculature
• growth-promoting effects of cardiac and vascular tissue

Question 25

Whats the effect of aldosterone?

Answer 25

Increased Na+ retention and (H2O)

Increased K+ excretion

Question 26

What triggers increased aldosterone production?

Answer 26

• Increased potassium
• Angiotensin 2
• minor effect from ACTH

Question 27

What happens in primary hyperaldosteronism?

Answer 27

Associated with benign of adrenal cortex. Associated with hypertension

Question 28

Secondary hyperalodsteronism cause?

Answer 28

Excessive response of the body in heart and liver failure

Question 29

What are the sympatho-adrenal and RAS responding to?

Answer 29

Stress

e.g. fluid loss

Question 30

What does activation of RAS and sympatho-adrenal systems do?

Answer 30

Increased HR
Increased BP
Increased Na+/Water retention

To decrease fluid loss:

• increased coagulation
• decreased fibrinolysis
• increased platelet activation