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CVS > Nervous and hormonal control > Flashcards

Nervous and hormonal control Flashcards

1
Q

What do intrinsic controls regulate?

A

o Regulate local blood flow to organs/tissues

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2
Q

Why are intrinsic controls important?

A

o Important – regional hyperaemia (increase in blood flow)

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3
Q

What do extrinsic controls regulate?

A

o Regulate TPR to control blood pressure

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4
Q

What is the sympathetic vasoconstrictor system?

A

The most widespread and important extrinsic control

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5
Q

Stimulation of sympathetic vasoconstrictor nerves

A

1) An AP moves down the axon and arrives at a varicosity
2) Depolarisation at the varicosity activates voltage gated Ca2+ channels
3) Ingress of Ca2+ causes release of neurotransmitters – mainly noradrenaline
4) NA diffuse to the vascular smooth muscle cells where it binds mainly
a. α1 – contraction
b. α2 – contraction
c. β2 – relaxation
i. Modulation of responses in both constriction and dilation
5) The noradrenaline is then taken up again and recycled or broken down
- Adrenaline from the adrenals and released into the circulation can also act at α1 or β2 receptors

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6
Q

How is release of NA modulated?

A
  • Release of NA can be modulated by Angiotensin II acting on AT1 receptor increasing NA release
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7
Q

What does vasoconstriction prevent?

A
  • Metabolites prevent vasoconstriction to maintain blood flow; K+, adenosine, histamine & serotonin etc. feedback and inhibit NA release
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8
Q

What can NA also do to its own release?

A
  • NA can also negatively feed back itself via α2 receptors to limit to its own release
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9
Q

What are sympathetic vasoconstrictor nerves controlled by?

A

Controlled by brainstem:
o Rostal Ventrolateral Medulla (RVLM) – this is controlled by other areas
o Caudal Ventrolateral Medulla (CVLM) & hypothalamus
 Provides central control of blood flow/blood pressure

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10
Q

What does the sympathetic vasoconstrictor nerves mostly innervate?

A
  • Innervate most arterioles & veins of the body
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11
Q

What is the sympathetic nerve activity?

A

o Sympathetic nerve activity is tonic (1 action potential per second)

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12
Q

What does tonic activity set?

A

o Tonic sympathetic activity sets vascular tone

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13
Q

What are the main roles of sympathetic vasoconstrictor nerves?

A

Contract resistance arterioles

Produces vascular tone which allows vasodilation/increased blood flow to occur, controls TPR
Distinct RVLM neurones-sympathetic pathways innervate different tissues

Switching on vasoconstriction in some vessels and off in other vessels (producing vasodilation)
E.g. exercise, increased sympathetic nerve stimulation to GI (less blood flow), reduce sympathetic nerve stimulation to skin (more blood flow, cool down).

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)

Control TPR
Maintains arterial BP and BF to the brain/myocardium as; Pa = CO x TPR

Controls venous blood volume

Venoconstriction leads to decreased venous blood volume which increases venous return, this increases SV via Starling’s law

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14
Q

What do a few specialised tissues contain?

A

A few specialised tissues contain vasodilator nerves, as well as vasoconstrictor nerves

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15
Q

What is the normal function of vasodilator nerves?

A

Normally have a specific function controlling a specific vascular bed rather than global functions

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16
Q

When does vasodilation usually occur?

A

Vasodilatation usually occurs as the vascular tone produced by sympathetic vasoconstrictor nerves is inhibited

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17
Q

Proportion of sympathetic to parasympathetic vasodilator nerves

A

Mainly parasympathetic vasodilator nerves

A few sympathetic vasodilator nerves

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18
Q

Parasympathetic vasodilator nerves(Salivary gland)

A

Release Ach and Vasoactive Intestinal Peptide (VIP)

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19
Q

Parasympathetic vasodilator nerves(Pancreas and intestinal mucosa)

A

Release VIP

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20
Q

What do both salivary glands, pancreas and intestinal mucosa need?

A

Both of the above tissues need high blood flow to maintain fluid secretion

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21
Q

What do Ach/VIP act on?

A

Ach/VIP act on endothelium to cause the release of NO – vasodilation

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22
Q

What does the release of NO in erectile tissue cause?

A

Release NO – the release of NO by parasympathetic nerves causes the production of cGMP which leads to vasodilation

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23
Q

What enhances the effect of NO in erectile tissue and how?

A

Sildenafil (Viagra) enhances this effect of NO by inhibiting the breakdown of cGMP by phosphodiesterase-5

24
Q

Sympathetic(Skin(Sudomotor fibers))

A

Release Ach and VIP which causes vasodilation via NO
It is associated with sweating
Increased blood flow causes more sweat and also allows heat loss via the skin

25
Q

What also has controls over sudomotor fibers?

A

Emotional centres in the brain have some control over these fibres

26
Q

How are C fibres stimulated?

A

Stimulation of sensory axon reflex (C-fibres) by trauma, infection etc.

27
Q

What is released when C fibers are stimulated?

A

Release substance P or calcitonin gene-related peptide (CGRP)

28
Q

What is released when substance P or CGRP act on mast cells?

A

Act on mast cells to release histamine

29
Q

What else does substance P or CGPR act on?

A

Act on endothelium and vascular smooth muscle

30
Q

What do both endothelium and vascular smooth muscles produce?

A

Both produces vasodilation called “Flare” in skin

31
Q

What is inflammation part of?

A

Inflammation is part of the Lewis Triple Response

32
Q

What is the lewis triple response?

A

1) Local redness
2) Wheal
3) Flare

33
Q

Example of hormonal vasoconstrictors

A

Adrenaline
Angiotensin II
Vasopressin (Anti-Diuretic Hormone, ADH)

34
Q

Example of hormonal vasodilators

A

Atrial Natriuretic Peptide (ANP)

35
Q

Where is adrenaline released from?

A

Adrenaline is released from the adrenal medulla

36
Q

Via what action is adrenaline released and when?

A

via the action of Ach on nicotinic receptors during:
Exercise
Flight-Fight-Fear response (increase sympathetic drive)
Hypotension (baroreceptor flex)
Hypoglycaemia

37
Q

What are the main roles of adrenaline?

A

metabolic and CVS effects

38
Q

Effects of adrenaline?

A

Vasodilation of coronary and skeletal muscle arteries

39
Q

What receptors do skeletal muscles and coronary arteries have more of?

A

Skeletal muscle and coronary arteries have more β2 than α1 adrenoreceptors

40
Q

What does adrenaline have a higher affinity for and where does it mainly act??

A

Adrenaline has a higher affinity for β over α, mainly acts at β2 to dilate vessels

41
Q

What does noradrenaline have a higher affinity for and where does it mainly act?

A

Noradrenaline has a higher affinity for α, mainly acts as α1 receptors to constrict vessels

42
Q

Adrenaline vs Noradrenaline

A

Refer to table

43
Q

Effect of iv adrenaline

A
  • Effect on heart(Beta 1 )
  • CO goes up and TPR goes down so not much effect on BP
  • Lower affinity for alpha 1 than beta 2, causing skeletal muscles arteriole to dilate, decreasing TPR
44
Q

RAAs system

A
  • Low blood pressure, stimulation of sympathetic nerve and low NaCl load are a stimulus
  • This results in the release of renin which combines with angiotensinogen
  • Renin causes antiogensinogen to undergo proteolysis to form angiotensin I
  • Angiotensin I converted into angiotensin II by ACE(enzyme)
  • Angiotensin II causes vasoconstriction which raises TPR increasing BP, stimulating sympathetic nerves
  • Angiotensin II activates the production of aldosterone which raises blood volume
45
Q

How is hypothalamus response stimulated?

A

Hypothalamus response is stimulated by an increase in osmolarity
i.e. dehydration or low blood volume

46
Q

What does vasopressin or ADH released cause?

A

Vasopressin or ADH released from the posterior of the pituitary gland that is controlled causes vasoconstriction (also increases the renal absorption of water)

47
Q

What do stretch receptors in left atrium have ?

A

Stretch receptors in the left atrium have continuous signals causing firing in the NTS
This sends out inhibitory nerves to the CVLM

48
Q

What does the CVLM stimulate and causes the release of what?

A

The CVLM stimulates the pituitary to release vasopressin so stretching of the heart inhibits this.

49
Q

What does dehydration or haemorrhafe result in?

A

NTS inhibition is switched off and CVLM stimulates vasopressin

50
Q

What is NTS in relation to CVLM?

A

NTS is the thermostat that sets the level at which the CVLM is inhibited

51
Q

What is ANP released by?

A

Released by specialised atrial myocytes

52
Q

Where does ANP act at and what does it increase?

A

Act at NP receptors on vascular smooth muscle cells increasing the cGMP pathway (like NO)

53
Q

What does systemic vasodilation oppose?

A

Systemic vasodilation – opposes action of noradrenaline, RAAS, ADH

54
Q

What does dilation of renal afferent arteriole increase?

A

Dilatation of renal afferent arteriole increases GFR

55
Q

What happens as renal afferent arteriole dilate?

A

Na+ and H2O excretion by the kidney are increased and blood volume goes down decreasing the release and/or actions of aldosterone, renin & ADH

CVS (17 decks)

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