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SGUL - Physiology 1 > Nervous and Hormonal Control of Vascular Tone > Flashcards

Nervous and Hormonal Control of Vascular Tone Flashcards

1
Q

Give examples of three molecules that cause vasoconstriction

A
  • Adrenalin
  • Angiotensin II
  • Vasopressin
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2
Q

What might trigger vasoconstriction?

A

Low blood pressure

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3
Q

Where is ANP (atrial natriuretic peptide) secreted from?

A

Specialised atrial myocytes

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4
Q

What is the effect of ANP on vascular tone?

A

Vasodilation
- Opposes action of adrenalin, vasopressin etc.

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5
Q

What might stimulate the release of ANP?

A
  • Stimulation of stretch receptors
  • This is triggered by increased atrial filling pressure/ increased blood volume
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6
Q

What receptors does ANP act on?

A

The receptors on vascular smooth muscle e.g arterioles, blood vessels etc.

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7
Q

Where are the ANP receptors in the kidneys found?

A

Afferent arterioles

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8
Q

Suggest the effect of stimulation of the kidney ANP receptors.

A
  • Increased volume of blood filtered by kidney (i.e greater GFR)
  • Increased filtration by the kidney
  • Reduced blood volume
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9
Q

Where is vasopressin synthesised and released from?

A

SYNTHESISED - hypothalamus
RELEASED FROM - vesicles in posterior pituitary

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10
Q

What are the two ways in which vasopressin maintains blood pressure and increase blood volume?

A
  • Vasoconstriction
  • Reabsorption of fluid from kidney (reduced filtration of blood)
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11
Q

Define diuresis

A

Filtration of blood at the kidneys
- Vasopressin opposes this action

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12
Q

Outline the steps involved in the release of vasopressin.

A
  • Stretch receptors in the aortic arch and on the left atrium continually send signals to an area of the medulla - the nucleus tractus solitarius (NTS).
  • The NTS then sends an inhibitory signal to another area of the medulla - the caudal ventrolateral medulla (CVLM).
  • The CVLM sends signals to the posterior pituitary to stimulate the release of ADH
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13
Q

How is vasopressin release inhibited when blood volume is low/pressure is normal?

A
  • Stretching causes signal to be sent to NTS
  • Inhibitory signal sent to CVLM
  • Reduced release of vasopressin
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14
Q

How is stretching affected when blood pressure/blood volume is reduced?

A

Stretching is reduced

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15
Q

What is the consequence of reduced stretching of the heart?

A
  • Reduced signal sent to NTS
  • Reduced inhibitory signal sent to CVLM
  • Increased CVLM signal to hypothalamus
  • Vasopressin is released
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16
Q

What are two other ways in which vasopressin may be released?

A
  • Detection of increased osmolarity of blood e.g due to dehydration
  • Also stimulated by angiotensin II release
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17
Q

What stimuli may cause the release of renin from kidneys?

A
  • Decrease in renal blood flow
  • Reduction in amount of Na+ being filtered really
  • Increased sympathetic nervous system activity
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18
Q

What is the purpose of renin?

A
  • Protease enzyme
  • Cleaves precursor, angiotensinogen to active molecule angiotensin I
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19
Q

Where is angiotensinogen found and produced?

A

PRODUCED - in liver
FOUND - in circulation

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20
Q

Compare the amino acid length of angiotensinogen to that of angiotensin I.

A

ANGIOTENSINOGEN - 453 amino acids
ANGIOTENSIN I - 10 amino acids

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21
Q

When is angiotensin I converted to angiotensin II?

A

As angiotensin I passes through the lungs

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22
Q

How long is angiotensin II?

A

8 amino acids

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23
Q

Which protease enzyme catalyses the conversion of angiotensin I to angiotensin II?

A

ACE (angiotensin converting enzyme)

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24
Q

Why do angiotensin II concentrations rise very rapidly?

A

Each molecule of renin and ACE can catalyse the cleavage of a large number of substrates

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25
Q

What are the three major effects of angiotensin II?

A
  • Acts as a vasoconstrictor and increases TPR
  • Stimulates sympathetic nervous activity
  • Stimulates aldosterone release
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26
Q

What are the effects of increasing TPR and sympathetic nervous activity?

A

Greater blood pressure

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27
Q

What is the effect of releasing aldosterone?

A
  • Greater reabsorption of sodium ions and greater water retention
  • Increases blood volume
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28
Q

Angiotensin II also acts on the hypothalamus. Suggest a possible effect.

A

Triggering vasopressin release

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29
Q

How might an intravenous injection of adrenalin influence heart rate and cardiac output?

A
  • Adrenalin has a high affinity for β-receptors
  • Binding to β-receptors causes an increase in heart rate and therefore, increase in cardiac output
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30
Q

How might an intravenous injection of adrenalin influence TPR?

A
  • Binding to skeletal muscle β2-receptors causes vasodilation
  • May activate some α1-receptors causing vasoconstriction (this response is lower - due to higher affinity for β-receptors)
  • TPR goes down
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31
Q

What is the overall effect on blood pressure by an intravenous injection of adrenalin?

A

Very little change in blood pressure

32
Q

How might an intravenous injection of noradrenaline influence TPR and blood pressure?

A
  • High affinity for α-receptors
  • Binding to α1-receptors causes vasoconstriction
  • TPR increases and therefore blood pressure rises
33
Q

How might an intravenous injection of noradrenaline influence heart rate and cardiac output?

A
  • High BP stimulates baroreceptors
  • Reduced sympathetic signals to β1-receptors
  • Decrease in heart rate, therefore decrease in cardiac output
34
Q

When might an intravenous injection of noradrenaline be administered clinically?

A
  • During hypotension (reduction in blood pressure)
  • To raise blood pressure without damaging the heart
35
Q

In most tissues which receptors mediate vasoconstriction and vasodilation?

A

VASOCONSTRICTION - α1adrenoreceptors
VASODILATION - β2 adrenoreceptors

36
Q

In skeletal muscle, adrenaline causes vasodilation and noradrenaline causes vasoconstriction. Suggest a reason for this difference.

A
  • Difference in receptor affinity
  • Adrenaline has higher affinity for β2-receptors and so causes vasodilation
  • Noradrenaline has higher affinity for α1-receptors and so cause vasoconstriction
37
Q

Where is adrenaline released from?

A

Adrenal medulla

38
Q

Outline how adrenaline is released from the medulla.

A
  • Released in response to sympathetic nervous system through splanchnic nerves passing to adrenal glands
  • ACh released at preganglionic fibres and acts on nicotinic ACh receptors. This stimulates adrenaline release
39
Q

Outline the effects of adrenaline (along with which receptor is stimulated)

A
  • Vasodilation of coronary and skeletal muscle arteries (β2)
  • Stimulation of heart rate and contractility (β1)
  • Glucose metabolism (e.g glycogenolysis) (β3)
40
Q

What are the purpose of sensory vasodilator fibres/C-fibres?

A

Convey pain signals to the brain when stimulated by trauma

41
Q

What are the main effects of sensory vasodilator fibres?

A
  • Stimulation up the dorsal root ganglia and up spinal cord
  • Stimulation of axon collaterals
42
Q

What would be the effect of stimulating axon collaterals?

A
  • Release of Substance P which cause vasodilation of blood vessels, degranulation of mast cells
  • OVERALL EFFECT: heavy vasodilation close to site of trauma
43
Q

Outline the purpose of the inflammatory response with regards to trauma

A

Increased delivery of immune cells to site of trauma to kill invading pathogens

44
Q

The Lewis Triple effect lists three effects that occur due to vasodilation.

Outline these effects.

A
  • Local redness due to vasodilation
  • ‘Flare’ - further redness in surrounding area due to arteriole dilation
  • Wheals - exudation of extracellular fluid from capillaries/venules
45
Q

Why is vasodilation important for the GI tract and salivary glands?

A
  • High blood flow needed to maintain fluid secretion - so both GI tract and glands release ACh, VIP etc.
  • Blood flow for secretory areas maintained by ACh
  • VIP increases gut secretions and motility
46
Q

How does NO induce vasodilation?

A

Causes conversion of GTP to cGMP which causes vasodilation

47
Q

What is the importance of having sympathetic vasodilators during thermoregulation?

A
  • Release ACh, VIP to cause vasodilation and increase blood flow
  • Greater blood flow means greater heat loss and greater sweating at high temperatures
  • Vasoconstriction would limit cooling and sweat production
48
Q

TRUE OR FALSE - Specific vasodilator nerves are dominantly sympathetic

A

FALSE
- There are only a few sympathetic vasodilator nerves
- Most are parasympathetic/cholinergic fibres

49
Q

Name and outline a possible mechanism for vasodilation caused by the parasympathetic nervous system

A
  • Parasympathetic fibres release ACh which bind to M3 receptors on smooth muscle/endothelium
  • Activation of these receptors cause formation of NO
  • This causes conversion of GTP to cGMP
    RESULT: Vasodilation
50
Q

A patient has a cholinomimetic drug administered. This causes a mixture of both vasoconstriction an vasodilation. Suggest why.

CHOLINOMIMETIC DRUGS - drugs which mimic the action of acetylcholine

A
  • ACh can also cause vasoconstriction e.g through M2 receptors
  • ACh also causes vasodilation through M3 receptors
51
Q

Suggest a possible effect of endothelial damage on vascular tone.

A
  • Disrupted release of NO
  • Reduced vasodilation/increased vasoconstriction
52
Q

What causes vasodilation of cerebral arteries?

A
  • Activation of M5 receptors by ACh
53
Q

How does venoconstriction influence cardiac output?

A
  • Decreased venous blood volume
  • Greater venous return
  • Greater stretching and greater force of contraction (through Starling’s Law)
  • Greater cardiac output
54
Q

What is the effect of vasoconstriction of arterioles?

A
  • Reduced blood pressure downstream
  • Reduced hydrostatic pressure at capillaries
  • Greater reabsorption of fluid from interstitial fluid
55
Q

What is the effect of changing the vascular tone of arterioles?

A
  • Vasoconstriction will increase TPR - vasodilation will do the opposite
  • Arterial blood flow to areas such as the brain and myocardium is maintained
56
Q

Describe the effect of having multiple sympathetic pathways on vasoconstriction.

A
  • Allows blood flow to be directed where it is needed
  • Allows blood pressure and flow to be tailored to specific situations
  • During hot conditions, reduced stimulation to skin - greater blood flow, greater heat loss
57
Q

What is the effect of the RVLM?

A
  • Works with other centres such as the CVLM to coordinate control of the CVS and regulate activity of preganglionic fibres
  • Uses nervous information to produce sympathetic-mediated responses to control blood pressure and flow based on needs
58
Q

Outline the general effect that sympathetic stimulation has on the blood vessels

A

Binding of noradrenaline to α1adrenoreceptors

59
Q

How can vasodilation be caused through the sympathetic nervous system?

A
  • Reduce sympathetic stimulation
  • Reduce vascular tone. RESULT: vasodilation
60
Q

Give a clinical example of where a decrease in sympathetic activity is beneficial

A

AMLODIPINE - used to treat hypertension
- Causes reduced vascular tone
- Causes greater vasodilation

61
Q

How is noradrenaline released from the nerve?

A
  • Action potential stimulates opening of VGCCs
  • Increased calcium influx
  • Greater intracellular [Ca2+] which triggers release of vesicles containing noradrenaline
62
Q

Give an example of a stimulus that would increase noradrenaline release.

A
  • Stimulated by binding of angiotensin II to AT1 receptor
63
Q

Give an example of a stimulus that would decrease noradrenaline release.

A
  • Binding of metabolites such as H+
  • Binding of vasodilators such as histamines
64
Q

What is the effect of increasing noradrenaline release?

What is the effect of decreasing noradrenaline release?

A

INCREASE - increase in vascular tone and vasoconstriction
DECREASE - vasodilation

65
Q

How can noradrenaline limit its own release?

A
  • Important when the concentration of noradrenaline is very high
  • Noradrenaline binds to α2 adrenoreceptors
  • This inhibits adenylate cyclase
  • This prevents action of PKA
  • Reduced phosphorylation of calcium ion channels
  • Reduced release of noradrenaline
66
Q

Where is noradrenaline released from?

A

Swellings in sympathetic vasoconstrictor nerves
- These swellings are called ‘varicosities’

67
Q

Outline how noradrenaline causes vasoconstriction.

A
  • Action potential moves down axon and arrives at varicosity
  • Varicosity becomes depolarised and VGCCs open
  • Increase in intracellular [Ca2+] which causes noradrenaline release
  • Binds to α1 adrenoreceptors on vascular smooth muscle and causes vasoconstriction
  • Noradrenaline is then taken up again or hydrolysed
68
Q

What is the effect of having multiple varicosities?

A

Greater area of smooth muscle affected

69
Q

Where do the preganglionic fibres originate in the sympathetic nervous system?

A

The IML of the spinal cord

70
Q

What do the preganglionic fibres travel to?

A
  • Ganglia - synapse with a postganglionic fibre
71
Q

What occurs at the ganglia?

A

Release of ACh which binds to nicotinic ACh receptors

72
Q

Noradrenaline is released by most postsynaptic neurones.

Outline two of its effects.

A

VASOCONSTRICTION - binding to α1 adrenoreceptors
VASODILATION OF SOME BLOOD VESSELS - binding to β2 adrenoreceptors

73
Q

What is the effect of sympathetic innervation of the adrenal medulla?

A

Triggers adrenalin release which can activate α1 and β2 receptors

74
Q

What is the difference between arterioles and veins?

A

ARTERIOLES - resistance vessels - affect TPR
VEINS - capacitance vessels - hold onto a reservoir of blood that can be mobilised when needed

75
Q

What is the difference between intrinsic and extrinsic control of blood flow?

A

INTRINSIC - local control of blood flow
EXTRINSIC - dependent on external sources such as hormones

76
Q

Give examples of intrinsic controls of blood flow.

A
  • Physical factors e.g temperature and stress
  • Local metabolites e.g histamines, endothelins
77
Q

Give examples of extrinsic controls of blood flow.

A
  • Hormones
  • Innervation by vasodilator and vasoconstrictor nerves

SGUL - Physiology 1 (68 decks)

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