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CVS > 8. Sympathetic Nervous and Renin Angiotensin Sytems > Flashcards

8. Sympathetic Nervous and Renin Angiotensin Sytems Flashcards

1
Q

Which regions of the CNS do the sympathetic and parasympathetic pathways come from?

A
  • Sympathetic - thoracolumbar

* Parasympathetic - craniosacral

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2
Q

What do baroreceptors do and where are they found?

A
  • Pressure sensors
  • Increased baroreceptor firing => increased parasympathetic activity
  • Sympathetic effect to cause vasodilation - reduced BP
  • Found in the Aortic Arch and Carotid arteries
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3
Q

Which neurotransmitter do all parasympathetic nerve terminals release?

A

Acetylcholine

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4
Q

What is the neurotransmitter in the paravertebral sympathetic ganglion?

A

Acetylcholine

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5
Q

What is the neurotransmitter at the effector sympathetic nerve terminal?

A

Noradrenaline

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6
Q

What part of the body acts as a specialised post-ganglionic neurone, releasing adrenaline/noradrenaline?

A

Adrenal medulla

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7
Q

What do post-ganglionic fibres to the sweat glands release?

A

Acetylcholine

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8
Q

What type of hormones are noradrenaline and adrenaline?

A

Catecholamines

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9
Q

How is noradrenaline synthesised and released?

A
  • Tyrosine enters terminal varicosity - small nodule at the end of the sympathetic release
  • Converted into dopamine which enters vesicle - dopamine => noradrenaline
  • The granular vesicles fuse with varicosity membranes and are exocytosed - active (ATP)
  • Reuptake and removal of noradrenaline
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10
Q

What are the 2 methods to remove noradrenaline from the cleft?

A

1) Goes back to the neurone that released it

2) Taken up by extraneuronal cells and broken down by COMT (Catechol-O-Methyl Transferase) and MAO (Monoamine Oxidase)

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11
Q

How are adrenoreceptors subdivided?

A
  • Alpha - excitatory effects on smooth muscle
  • Beta - relaxant effects on smooth muscle + stimulatory effect on heart (inotropic and chronotropic i.e. increase force of contraction and heart rate)
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12
Q

How are beta receptors subdivided?

A
  • Beta 1 - cardiomyocytes, smooth muscle of GI tract
  • Beta 2 - vasculature, bronchi, uterine smooth muscle
  • Beta 3 (recently added) - fat cells, possibly on smooth muscle of GI tract
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13
Q

How are alpha receptors subdivided?

A
  • Alpha 1 - located post-synaptically (predominantly on effector cells), mediate constriction of resistance vessels in response to sympathomimetic amines - BP regulation
  • Alpha 2 - located pre-synaptically, their activation by released transmitter causes negative feedback inhibition of further transmitter release (some are post-synaptic on VSMCs)
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14
Q

How do Alpha 1 Adrenoreceptors work?

A
  • Signal transduction via G protein
  • Activation of receptor => activation of Phospholipase C
  • PLC convert PIP2 => IP3
  • Release of calcium from intracellular stores
  • Contraction
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15
Q

How are Beta and Alpha 2 adrenoreceptors coupled?

A
  • Beta receptors are coupled with Adenylate Cyclase
  • Adenylate Cyclase increases levels of cAMP
  • cAMP is an inhibitor in smooth muscle and platelets
  • cAMP activates cardiomyocytes
  • Alpha 2 receptors are also calcium releasing receptors
  • However, it inhibits the Adenylate Cyclase
  • Reduced cAMP => reduced calcium release
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16
Q

Which substances are involved in anaphylaxis and what does it cause?

A
  • Release of vasodilators
  • Bronchoconstriction
  • Adrenaline activates all the receptors you need to counteract the effects of this
17
Q

What is dopamine?

A
  • A precursor for the catecholamines that have some effects on Alpha 1 and Beta 1 receptors
  • Has its own receptors in the vasculature and kidneys
18
Q

Which 2 synthetic drugs can be used to examine what the adrenoreceptors do?

A
  • Isoprenaline (also treatment for asthma)
  • Phenylephrine
  • They bind to different receptors and can determine the different contribution of the receptors to cardiovascular changes
19
Q

What effects do noradrenaline, adrenaline and isoprenaline have on blood pressure?

A
  • Noradrenaline - massively increases BP (vasoconstricton increasing TPR)
  • Adrenaline - increases BP to a lesser extent due to beta effects which counter alpha effects, vasodilator - decreases DBP
  • Isoprenaline - beta agonist, no vasoconstriction - no increase in resistance
20
Q

What effects do noradrenaline, adrenaline and isoprenaline have on heart rate?

A
  • Noradrenaline - reflex bradycardia due to vasoconstriction => increase BP => increased baroreceptor firing frequency => deactivation of the sympathetic innervation of the heart => increased activity of vagus nerve => reduced heart rate
  • Adrenaline - potent effect on beta receptors on cardiomyocytes => increase heart rate
  • Isoprenaline => more direct increase in heart rate (not counteracted by alpha effects peripherally)
21
Q

What is the response of the skin, visceral and renal vascular bed to catecholamines?

A
  • Noradrenaline - constriction
  • Adrenaline - constriction
  • Isoprenaline - none (or dilation)
22
Q

What is the response of the coronary vascular bed to catecholamines?

A
  • Dilation

* alpha, beta 1 receptors

23
Q

What is the response of the skeletal muscle vascular bed to catecholamines?

A
  • Noradrenaline - constriction
  • Adrenaline - dilation
  • Isoprenaline - dilation
  • alpha, beta 2 receptors
24
Q

Which adrenoreceptors can kidney cells use for stimulation?

A

Stimulated through the sympathetic nervous system, using Beta 1 receptors

25
Q

Which 3 major elements regulate renin release?

A
  • Amount of sodium - reaches the macula densa (near the glomerulus), less sodium - more renin
  • Blood pressure - in preglomerular vessels, lower BP - more renin
  • Beta Receptor Activation - sympathetic response, more beta receptors activated - more renin

• Usually a response to stress situations

26
Q

How can renin release be manipulated pharmacologically?

A
  • Blocking Angiotensin II receptors
  • ACE inhibitors (although this pathway can be bypassed)
  • Beta blockers stop renin release in the kidneys
  • Loop diuretics indirectly increases renin secretion because less sodium gets to the kidney
  • NSAIDs can increase renin release (unintentionally)
27
Q

What are AT1 receptors?

A
  • Angiotensin II Type 1 receptors
  • G-protein coupled receptors (Gi and Gq)
  • Also couples with Phospholipase A2
  • Located in blood vessels, brain, adrenals, kidneys and heart
  • Activation => increased BP
28
Q

What are the effects of Angiotensin II in peripheral resistance?

A

• Rapid pressor response

  • direct vasoconstriction
  • enhanced action of noradrenaline (increased release, decreased uptake)
  • increased sympathetic discharge
29
Q

What are the effects of Angiotensin II in renal function?

A

• Slow pressor response

  • weeks/months
  • increases sodium reabsorption into proximal tubule - increased water retention
  • aldosterone synthesis in adrenal cortex
  • renal vasoconstriction
  • enhanced noradrenaline effects
30
Q

What Vascular and Cardiac effects does Angiotensin II have (haemodynamic and non-haemodynamic)?

A

Haemodynamic
• Increased preload and afterload
• Increased vascular wall tension

Non-Haemodynamic
• Increased expression of proto-oncogenes
• Increased production of growth factors
• Increased synthesis of extracellular matrix proteins
=> bigger, less efficient heart (hypertrophy and remodelling)

31
Q

What are chymases?

A
  • Enzymes which convert Angiotensin I (or even angiotensinogen) to Angiotensin II
  • No way to block them at the moment
32
Q

What changes when you block ACE?

A
  • Less Angiotensin II

* More bradykinin

33
Q

What effects do AT1 antagonists block?

A
  • Pressor effects
  • Stimulation of noradrenaline system
  • Secretion of aldosterone
  • Effects on renal vasculature
  • Growth-promoting effects of cardiac and vascular tissue
  • Uricosuric effect
  • Avoid angiooedema
34
Q

What can cause angiooedema?

A
  • ACE inhibitors
  • ACE can no longer inactivated bradykinin
  • Build up of bradykinin
  • Swelling
35
Q

What are the main triggers for aldosterone production?

A
  • Increased potassium
  • Angiotensin II
  • Minor effect from ACTH
36
Q

What effect does aldoesterone have on blood content?

A
  • Increased potassium (and H+) excretion
  • Increased sodium (and water) retention
  • This increases BP
37
Q

Where can aldosterone receptors be found?

A
  • Kidneys
  • Brain
  • Heart
  • Blood vessles
38
Q

What are the effects of primary and secondary hyperaldosteronism?

A 
• Primary Hyperaldosteronism
- associated with benign tumours of the adrenal cortex
- hypertension
- no oedema
• Secondary Hyperaldosteronism
- excessive response of the body in heart and liver failure
- low/normal blood pressure
- lots of oedema
39
Q

How do the sympatho-adrenal and renin-angiotensin systems respond to fluid loss (stress) and what are the problems with this?

A
  • Increase BP
  • Increase heart rate
  • Increase sodium/water retention
  • Increased coagulation
  • Decreased fibrinolysis
  • Increased platelet activation
  • Aim to maintain extracellular circulatory volume
  • Could lead to heart failure and hypertension

CVS (21 decks)

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