nervous and hormonal control of vascular tone Flashcards

1
Q

What are the 2 types of vascular control?

A
  1. Local control
    ○ Myogenic responses
    ○ Paracrine and autoregulation agents
    ○ Physical factors
2. Extrinsic control 
○ Parasympathetic 
○ Sympathetic 
○ Sensory vasodilator nerves 
○ Sympathetic vasoconstrictor nerves

Others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the importance of intrinsic controls?

A

Regulates local blood flow to organs and tissues

aka regional hyperaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the importance of extrinsic controls?

A
  1. Regulates TPR to control blood pressure
  2. Brain function selectively alters blood flow to organs/tissues where needed
    For example more blood flow is required to muscles during exercise
  3. Nerves:
    • Vasodilator (acetylcholine + nitric oxide)
    • Vasoconstrictor (noradrenaline)
  4. Hormones
    • Vasodilator (ANP)
    - Vasoconstrictor (vasopressin + adrenaline + angiotensin II)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the most widespread and important extrinsic control?

A

Sympathetic vasoconstrictor system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe how the sympathetic innervation of arterioles leads to NA release and explain the different outcomes

A
  1. An action potential moves down the axon and arrives at the varicosity; innervating the adventitia
    1. Depolarisation occurs at varicosity, activating the voltage gated calcium channels
    2. This causes an influx of calcium ions
    3. Influx of Ca2+ = release of neurotransmitter (noradrenaline-NA)
    4. NA diffuses to vascular smooth muscle, and binds to:
      • Mainly alpha-1 = contraction
      • Some alpha-2 = contraction
      • Some beta-2 = relaxation
      These responses are modulated during vasoconstriction and vasodilation
    5. NA is then taken back up again and is either recycled OR broken down
      Adrenaline that is released from the adrenal glands and released into the bloodstream can also act as alpha-1 or beta-2 receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe what happens at varicosity in detail

A

• Release of NA can be modulated by angiotensin II (+)
• Angiotensin II binds to AT1 receptors = increase in cAMP = increases calcium influx via voltage gated calcium channels = more NA released = increased vasoconstriction
• Some metabolites prevent vasoconstriction by negatively regulating cAMP = less NA release = less vasoconstriction = more blood flow
These metabolites include:
1. Serotonin
2. K+
3. Adenosine
4. Histamine
• NA can also inhibit it’s own release by binding to alpha-2 receptors

More NA = more vasoconstriction = less blood flow
Less NA = less vasoconstriction = more blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the sympathetic vasoconstrictor nerves controlled by?

A

Controlled by the brainstem
Rostral ventrolateral medulla (RVLM) – this is controlled by other areas, Caudal ventrolateral medulla (CVLM) & hypothalamus.
Provides central control of blood flow/blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What causes arteriole and venues vasoconstriction?

A

NA binds to alpha-1 receptors on vascular smooth muscle causing vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why is a decrease in sympathetic activity important?

A

Decrease in sympathetic activity producing vasodilatation is an important principle in pharmacological treatment
of cardiovascular disease, eg. Hypertension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the main roles of the sympathetic vasoconstrictor nerves

A
  1. Contract resistance arterioles
    Produces vascular tone allows vasodilatation/increased blood flow to occur, controls TPR.
    1. Distinct RVLM neurones-sympathetic pathways innervate different tissues
      Switching on vasoconstriction in some vessels and off in other vessels (producing vasodilation)
      eg. exercise, increased sympathetic nerve stimulation to GI (less blood flow), reduce sympathetic nerve stimulation to skin (more blood flow, cool down).
    2. Pre-capillary vasoconstriction
      Leads to downstream capillary pressure drop so increased absorption of interstitial fluid into blood plasma to maintain blood volume (important in hypovolemia).
    3. Control TPR
      Maintains arterial blood pressure and blood flow to brain/myocardium since Pa = CO x TPR
    4. Controls venous blood volume
      Venoconstriction leads to decreased venous blood volume increasing venous return, this increases stroke volume via Starling’s law.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is an example of a sympathetic vasodilator nerve?

A

Sensory vasodilator fibres (nociceptive C fibres)

However, body mainly uses parasympathetic vasodilator nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where are the parasympathetic vasodilator nerves founds?

A
  1. Salivary glands
    Release Ach and VIP
    1. Pancreas and intestinal mucosa
      Release VIP
      Both these tissues need high blood flow to maintain fluid secretion
    2. Male genitalia
      Release NO via parasympathetic nerves = production of cGMP = vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is Sildenafil and how does it affect parasympathetic vasodilator nerves?

A

Viagra

Enhances the effect of NO on erectile tissues by inhibiting breakdown of cGMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where are the sympathetic vasodilator nerves found and how do they work?

A

Skin

Release Ach and VIP = vasodilation via NO = increases blood flow = increase sweat= heat loss via skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the effect of the sympathetic vasoconstrictors on the skin?

A

Reduce blood flow = less sweat = limits heat loss

Emotional centres in the brain have control over the structures involved in blushing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the effect of stimulation of sensory (nociceptive C fibres) vasodilator fibres

A

The stimulation of the sensory axon reflex occurs by trauma and infection
They release a substance called substance P or calcitonin gene related peptide (CGRP)
This acts on mast cells to release histamine. It also acts on the endothelium and vascular smooth muscle
Both histamine and CGRP produce vasodilation = flare on skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do sensory vasodilator fibres release and act on?

A

Release: substance P + CGRP

Act on: mast cells + endothelium + vascular smooth muscle

18
Q

What is the effect of histamine or CGRP release from the sensory vasodilator fibres?

A

Flare on skin

19
Q

What is the lewis triple response?

A
  1. Local redness
    1. Wheal
    2. Flare
20
Q

Name some hormones that affect the control of circulation

A
1. Vasoconstrictors 
	• Adrenaline 
	• Angiotensin II 
	• Vasopressin (ADH)
	2. Vasodilator 
	• Atrial natriuretic peptide (ANP)
	3. Others
	• Insulin 
	• Oestrogen 
	• Relaxin
21
Q

Describe the release of adrenaline aka epinephrine

A

Adrenaline is released from the adrenal medulla via the action of Ach on nicotinic cholinergic receptors during:

Exercise

Fight or flight response (> sympathetic drive)

Hypotension (baroreflex receptor)

Hypoglycaemia

22
Q

Describe the main roles of adrenaline release

A

Metabolic and CVS effects
• Glucose metabolism (skeletal muscle glycogenolysis, fat lipolysis)
• Stimulation of heart rate and contractility during normal exercise
• Vasodilation of coronary and skeletal muscle artery

23
Q

Describe the effect of adrenaline and NA on most tissues such as GI tract and skin

A
NA = vasoconstriction 
Adrenaline = vasoconstriction
24
Q

Describe the effect of adrenaline and NA on skeletal muscle and coronary circulation

A
NA= vasoconstriction 
Adrenaline= vasodilation
25
Q

What receptor does adrenaline act on to dilate vessels

A

Adrenaline mainly acts on B2 receptors to dilate vessels

26
Q

What receptor does NA act on to constrict vessels

A

NA acts mainly on A1 receptors to constrict vessels

27
Q

What are the main receptors found on coronary arteries and skeletal muscle?

A

Beta 2 receptors

28
Q

What does stimulation of alpha1-Gq receptor result in?

A

Smooth muscle contraction

29
Q

What does stimulation of alpha1-Gi receptors result in?

A

Smooth muscle contraction

30
Q

What does inhibition of alpha1-Gi receptors result in?

A

Inhibition of neurotransmitter release

31
Q

What does the stimulation of B-Gs result in?

A
B1= heart contraction 
B2= smooth muscle relaxation = vasodilation
32
Q

Describe the effect of IV adrenaline on circulation

A

CO: increases
TPR: decreases
BP: not much effect
When given adrenaline, the heart rate increases. The CO increases HOWEVER because the TPR decreases (due to B2 receptor stimulation) there is not much effect on BP

33
Q

Describe the effect of IV NA on circulation

A
CO: decreases 
TPR: increases 
BP: increases
HR: decreases 
When given NA, there is a big increase in TPR (due to A1 receptor stimulation) which causes an increase in BP. Increased BP stimulates the baroreceptor reflex to decrease heart rate
34
Q

What is meant by RAAS?

A

Renin-angiotensin-aldosterone system

35
Q

Describe how RAAS responds to lowered blood pressure

A

Lowered BP = renin release from kidney via JGA (juxtaglomerular apparatus)
1. Renin triggers proteolysis of angiotensinogen —> angiotensin I
2. Lung releases ACE (angiotensin converting enzyme) converting angiotensin I—> angiotensin II
3. Angiotensin II triggers several responses which all lead to an increased blood pressure
• Angiotensin II directly causes vasoconstriction = raises TPR = increase in BP
• Angiotensin II causes the adrenal cortex to release a steroid hormone called aldosterone which increases kidney water retention via Na+ movement = raise in blood volume = increases BP
Angiotensin II also directly increases the body’s sympathetic response = increase BP

36
Q

What type of hormone is vasopressin?

A

ADH
Anti diuretic hormone
STOPS YOU PEEING

37
Q

How does the body respond to low blood volume (ie- low BP)

A

• Dehydration or low blood volume stimulated the hypothalamus response to release CVLM
• CVLM cause magnocellular neurons in SON and PVN to release vasopressin from the posterior pituitary gland
Vasopressin release = acts as ADH + causes vasoconstriction = increases BP

38
Q

How does the body respond to high blood volume (ie- high BP)

A

• Left atrial receptors and arterial baroreceptors send signals to the NTS in the brainstem
• NTS negatively regulates the release of CVLM by sending negative inhibitory signals
Inhibition of CVL = no ADH release = more urine released to lower blood volume = lowers BP

39
Q

What is ANP and what releases it?

A

Anti natriuretic peptide released by specialised atrial myocytes
Secreted by increased filling pressures which stimulate stretch receptors (left atrial receptors and arterial baroreceptors)

40
Q

Describe the mechanism of action of ANP

A

ANP act as receptors on vascular smooth muscle for things such as NO = increasing cGMP pathway = vasodilation

41
Q

Describe how ANP opposes RAAS, NA, and ADH

A

ANP = dilation of renal arterioles = increase in GFR
This means that sodium and water excretion is increases = blood volume decreases
Decrease in blood volume opposes action of NA, RAAS and ADH