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LSS 1- CVS > The Sympathetic Nervous System and the Renin Angiotensin System > Flashcards

The Sympathetic Nervous System and the Renin Angiotensin System Flashcards

1
Q

Where do the parasympathetic and the sympathetic region originate from?

A

Parasympathetic comes from the craniosacral region.

Sympathetic comes from the thoracolumbar region

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2
Q

Where the baroreceptors located?

A

Carotid sinus + aortic arch

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3
Q

What neurotransmitter do all parasympathetic neurones release?

A

Acetylcholine

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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

What are the two catecholamines?

A

Noradrenaline

Adrenaline

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6
Q

where does synthesis of noradrenaline occur.

A

Occurs in the TERMINAL VARICOSITY: this is a small nodule at the end of the sympathetic nerve.

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7
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 using Catechol-O Methyltransferase (COMT)

OR
into extraneuronal tissue.
Enzymes = Monoamine Oxidase (MAO)

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8
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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9
Q

what does it mean by stimulatory effect on the heart

A

it means that it increases the force of contraction (inotropic effect) and increases heart rate (chronotropic effect)

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10
Q

Where are beta 1 receptors located?

A

Heart Muscle

GI tract

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11
Q

What are the subdivision of BETA-receptors and where are they found?

A

Beta 1 receptors located on:

  • cardiomycocytes
  • smooth muscle of GI tract.

Beta 2:

  • Vasculature
  • Bronchi
  • uterine smooth muscle

Beta 3:

  • fat cells (brown fat)
  • possibly on the smooth muscle of the GI tract
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12
Q

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

A

Post-synaptic membrane - they mediate VASOCONSTRICTION

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13
Q

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

A

They are located on the presynaptic membrane and their activation by released transmitter causes NEGATIVE FEEDBACK inhibition of further transmitter release.
Some are post-synaptic on smooth muscle cells and cause VASOCONSTRICTION (like alpha 1 cells)

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14
Q

What is the coupling of alpha-1 adrenoreceptors

A

via G proteins.

  1. receptor is activated
  2. causes the activation of phospholipase C.
  3. PLC converts PIP2 to IP3 which leads to a release of calcium from intracellular stores.
  4. an increase in intracellular calcium in a muscle cell causes CONTRACTION

so activation of these receptors increases calcium levels and causes contraction.

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15
Q

What is coupling of beta adrenoreceptors and alpha 2 adrenoreceptors?

A

Beta receptors are coupled with adenylate cyclase which increases the levels of cAMP.

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16
Q

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

A

in SMOOTH MUSCLE and PLATELETS= cAMP which is an inhibitor so it prevents activation, makes smooth muscle RELAX and prevents platelet activation.
in CARDIOMYOCYTES= increase cAMP, like calcium, activates the cell- this is unique to cardiomyocytes

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17
Q

what are the effects in alpha 2 receptors

A

Alpha 2 receptors are also calcium releasing receptors but this is more to do with inhibition of adenylate cyclase

18
Q

what is anaphylaxis?

A

Is an extreme allergic reaction where you get release of vasodilators and bronchoconstriction.

19
Q

Which adrenoreceptors do noradrenaline and adrenaline act on?

A 
Noradrenaline = a1 + a2 + b1
Adrenaline = ALL the adrenoreceptors
20
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
21
Q

What is the effect of a) noradrenaline, b) adrenaline and c) isoprenaline on systolic BP, diastolic BP, mean (To calculate a mean arterial pressure, double the diastolic blood pressure and add the sum to the systolic blood pressure. Then divide by 3) BP and heart rate?

A 
Noradrenaline = increase, increase, increase, decrease 
Adrenaline = increase, decrease, increase, increase 
Isoprenaline = increase, decrease, same, increase
22
Q

what is the effect of noradrenaline?

A

Noradrenaline massively increases total peripheral resistance, therefore the blood pressure rises.
You may get Reflex Bradycardia, this occurs because of the baroreceptor loop: vasoconstriction causes an increase in blood pressure which increases the firing frequency of the baroreceptors leading to the deactivation of the sympathetic innervation of the heart and increased activity of the vagus nerve leading to a reduced heart.

23
Q

what is the effect of adrenaline?

A

Direct increase in heart rate.

Adrenaline has quite potent VASODILATOR which means that it decreases diastolic blood pressure.

24
Q

What is the effect of isoprenaline?

A

It is a pure BETA AGONIST. The effects of it are limited because it isn’t going to cause any vasoconstriction and hence resistance won’t change much.

25
Q

summarise the effects of noradrenaline, adrenaline, isoprenaline

A 
Noradrenaline= reflex bradychardia
adrenaline= direct increase in heart rate
isoprenaline= more direct increase in heart rate
26
Q

What three elements regulate renin release?

A

Amount of sodium reaching the macula densa cells. The less sodium there is, the more renin will be released.
Blood pressure in the pre-glomerular vessels. Depends on the pressure within the preglomerular vessels- the lower the blood pressure, the more renin is released.
Sympathetic activity can increase renin release: the more beta receptors are activated, the more renin is released.

27
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

28
Q

What type of receptor is an Angiotensin II Type 1 (AT1) receptor and what does it work to do?

A

G protein coupled receptors (Gi and Gq)

-it works to increase BLOOD pressure.

29
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

30
Q

What is the SLOW pressor response of angiotensin II?

A

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

31
Q

Describe the effects of angiotensin II on the heart.

A

Increased preload and afterload

Increased vascular wall tension

32
Q

Decribe the effects of non-heamodynamic effects of aldosterone?

A
  • increased expression of proto-oncogenes
  • increased production of growth factors
  • increased synthesis of extracellular matrix proteins
33
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

34
Q

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

A

Reduce the breakdown of bradykininso more bradykinin is left.

35
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

36
Q

What is the effect of angiotensin II type 1 receptor antagonist

A

you can get angioodema(Angioedema affects the deeper layers, including the dermis, subcutaneous tissue, the mucosa, and submucosal tissues)

37
Q

What are two main stimuli for aldosterone release?

A

Angiotensin II

Increased Potassium

38
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
39
Q

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

A

FLUID LOSS (e.g. severe haemorrhage)

40
Q

What is primary hyperaldosteronism and secondary hyperaldosteronism?

A

Primary hyperaldosteronism: associated with benign tumours of the adrenal cortex- this is associated with hypertension.
Secondary hyperaldosteronism: excessive response of the body in heart failure and liver failure- the phenotype is completely different.

Primary= high blood pressure + NO oedema

Secondary= low/normal blood pressure + LOTS of oedema.

LSS 1- CVS (21 decks)

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