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sem 2 CVS > Nervous and hormonal control of vascular tone > Flashcards

Nervous and hormonal control of vascular tone Flashcards

1
Q

what is vascular tone?

A

the degree of constriction experienced by a blood vessel relative to its maximally dilated state

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2
Q

what is the main thing that controls TPR?

A

vascular tone

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3
Q

what is a resistance vessel?

what is a capacitance vessel?

A 
resistance = arteriole
capacitance = vein
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4
Q

paracrine, autocrine and endocrine

A

paracrine = if a cell sends a signal to an adjacent cell

autocrine = if a cell sends a signal to itself

endocrine = if a cell signals another cell that is far away

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5
Q

vascular control can be controlled by 2 different types: what are they?

A

intrinsic/local control
-regulate local blood flow to organs/tissues

extrinsic control

  • regulates TPR to control blood pressure
  • brain function selectivity alters blood flow to organs according to need (e.g. during exercise, thermoregulation)
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6
Q

name the types of intrinsic control:

A
  • myogenic response (resistance vessels)
  • paracrine and autoregulation agents (NO, PG’s, endothelin, K+, H+) (both)
  • physical factors (both)
  • temperature (both)
  • sheer stress (both)
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7
Q

name the types of extrinsic control:

A
  • parasympathetic, sympathetic, sensory vasodilator nerves (resistance vessels)
  • sympathetic vasoconstrictor nerves (both)
  • adrenaline (both)
  • angiotensin II (both)
  • vasopressin (both)
  • ANP (atrial natriuretic peptide) (both
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8
Q

what is the myogenic response?

A

how the arteries and arterioles react to increase/decrease in BP

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9
Q

how do nerves affect vascular control?

A

o Vasoconstrictors – e.g. noradrenaline

o Vasodilators – e.g. Ach, NO

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10
Q

how do hormones affect vascular control?

A

o Vasoconstrictors – e.g. adrenaline, angiotensin II, vasopressin
o Vasodilators – e.g. anti-natriuretic peptide (ANP)

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11
Q

what is the most widespread and important extrinsic control?

A

Sympathetic Vasoconstrictor System

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12
Q

what in the role of the brain in terms of information from the nervous system?

A

nervous system information is integrated by the brain

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13
Q

how are arterioles constantly held between contraction and dilation?

A
  • constant sympathetic NA effect (pulse every sec) sending NA to the vessels- makes them want to constrict
  • at the same time, there is background production of NO by the endothelial cells in the vessels- makes them want to dilate
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14
Q

where does info from the CVLM in the brain go?

A

RVLM

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15
Q

what are the CVLM and RVLM?

A

2 sensors in the brain that integrate signals to the sympathetic nervous system, partly automatic but also process info from higher sensors in the brain

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16
Q

explain how sympathetic vasoconstrictor nerves work?

A

1) An AP moves down the axon and arrives at a varicosity (little pearl shape)
2) Depolarisation at the varicosity activates voltage gated Ca2+ channels

3) Entry of Ca2+ causes release of neurotransmitters – mainly NA
4) NA can bind to β1 receptors on heart which increases HR and SV
5) NA diffuses to the vascular smooth muscle cells where it binds mainly to:
a. α1 – contraction
b. α2 – contraction
c. β2 – relaxation
6) The NA is then taken up again and recycled or broken down

  • Adrenaline from the adrenal glands can be released into the circulation can also act at α1 (contraction) or β2 (relaxation) receptors on smooth muscle
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17
Q

how can the smooth muscle be constricted or relaxed?

A

NERVOUS - NA released due to depolarisation

HORMONAL - Adrenaline released from the adrenal glands

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18
Q

how can NA release be modulated?

A
  1. Angiotensin II
  2. Metabolites
  3. NA can negatively feedback itself
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19
Q

how does Angiotensin II affect NA release?

A

Angiotensin II acts on AT1 receptors, causing an increase in NA release and vasoconstriction, causing an increase in BP.

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20
Q

how do metabolites affect NA release?

A

Metabolites (inflammatory mediators) have their own channels on the varicosity, inhibiting release of NA and causing vasodilation- prevent vasoconstriction to maintain blood flow

K+, adenosine, histamine & serotonin inhibit NA release by decreasing cAMP levels

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21
Q

how can NA modulate itself?

A

NA can negatively feedback itself via α2 receptors to limit to its own release

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22
Q

where does lots of modulation occur?

A

at the neurotransmitter level at the varicosity

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23
Q

role of the CVLM?

A

provides central control of blood flow/blood pressure

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24
Q

what do sympathetic vasoconstrictor nerves do?

A

Innervate most arterioles & veins of the body

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25
Q

sympathetic nerve activity is tonic - what does this mean and why is it important?

A

tonic means 1 action potential per second

o Tonic sympathetic activity sets vascular tone

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26
Q

how does NA cause vasoconstriction of vascular smooth muscle?

A

NA activates α1 – adrenoreceptors on vascular smooth muscle cells causing vasoconstriction

27
Q

what is an important principle in the pharmacological treatment of cardiovascular diseases like hypertension?

A

decrease in sympathetic activity producing vasodilation

28
Q

list the main roles of sympathetic vasoconstrictor nerves:

A
  • Contract resistance arterioles
    o Produces vascular tone which allows vasodilation/increased blood flow to occur, controls TPR
  • Distinct RVLM neurones-sympathetic pathways innervate different tissues
    o Switching on vasoconstriction in some vessels and off in other vessels (producing vasodilation)
    o 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
    o Leads to downstream capillary pressure drop so increased absorption of interstitial fluid into blood plasma to maintain blood volume (important in hypovolemia)
  • Control TPR
    o Maintains arterial BP and BF to the brain/myocardium as; Pa = CO x TPR
  • Controls venous blood volume
    o Venoconstriction leads to decreased venous blood volume which increases venous return, this increases SV via Starling’s law
29
Q

what do a few specialised tissues contain?

A

vasodilator nerves, as well as vasoconstrictor nerves

30
Q

do vasodilator nerves usually have a specific or non specific function?

A

vasodilator nerves normally have a specific function controlling a specific vascular bed rather than global functions, located in specialist nervous areas

31
Q

why does vasodilation occur?

A

occurs because the vascular tone produced by sympathetic vasoconstrictor nerves is inhibited

32
Q

are the majority of vasodilator nerves sympathetic or parasympathetic

A

mainly parasympathetic vasodilator nerves

a few sympathetic vasodilator nerves

33
Q

where are the parasympathetic vasodilator nerves located and what are their roles?

A
  • Salivary glands
    o Release Ach and Vasoactive Intestinal Peptide (VIP)
  • Pancreas & Intestinal Mucosa
    o Release VIP
  • Both of the above tissues need high blood flow to maintain fluid secretion
    o Ach/VIP act on endothelium to cause the release of NO – vasodilation
  • Male genitalia (erectile tissue)
    o Release NO – the release of NO by parasympathetic nerves causes the production of cGMP which leads to vasodilation
    o Sildenafil (Viagra) enhances this effect of NO by inhibiting the breakdown of cGMP by phosphodiesterase-5
34
Q

where are the sympathetic vasodilator nerves located and what are their roles?

A

Skin (sudomotor fibres) release Ach, VIP causing vasodilatation via NO associated with sweating – increased blood flow causes more sweat and also allows heat loss via skin.

Emotional centres in brain have some control over these fibres, head, face, upper chest, involved in blushing

35
Q

what would sympathetic activity (vasoconstriction) do in the skin?

A

reduce blood flow, limit sweat production and limit cooling

36
Q

what are sensory (nociceptive C fibres) vasodilator fibres?

A

reflex, go from skin to brain

37
Q

what stimulates the sensory axon reflex (C-fibres)?

A

trauma, infection etc.

38
Q

what do these sensory fibres release?

A

substance P or calcitonin gene-related peptide (CGRP)

39
Q

where do the substances that the sensory fibres release act and what effect do they produce?

A
  • act on mast cells to release histamine
  • act on endothelium and vascular smooth muscle
  • both produce vasodilation called “Flare” in skin

-inflammation is part of the Lewis Triple Response
o 1) Local redness
o 2) Wheal
o 3) Flare

40
Q

what is the lewis triple response

A

Inflammation is part of the Lewis Triple Response
o 1) Local redness
o 2) Wheal
o 3) Flare

41
Q

in terms of hormonal control of circulation, name some hormones that cause vasoconstriction, increasing BP:

A

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

42
Q

in terms of hormonal control of circulation, name some hormones that cause vasodilators, decreasing BP:

A

o Atrial Natriuretic Peptide (ANP)

43
Q

name some other hormones that also effect vasculature:

A

o Insulin
o Oestrogen
o Relaxin

44
Q

where is adrenaline released from and what causes this release?

A
  • nerves supplying adrenal medulla release Ach
  • adrenaline is released from the adrenal medulla via the action of Ach on nicotinic receptors during:

o Exercise
o Flight-Fight-Fear response (increase sympathetic drive)
o Hypotension (baroreceptor flex)
o Hypoglycaemia- low BG level, breakdown of glycogen into glucose

45
Q

wha are the main roles adrenaline has in the body?

A
  • Main roles – metabolic and CVS effects

o Glucose mobilisation (skeletal muscle glycogenolysis, fat lipolysis)
o Stimulation of heart rate and contractility during normal exercise
o Vasodilation of coronary and skeletal muscle arteries

46
Q

do skeletal muscle and coronary arteries have more β2 or α1 adrenoreceptors?

A

more β2

47
Q

what type of receptor does adrenaline have a higher affinity for and where does it act?

A
  • adrenaline has a higher affinity for β over α, mainly acts at β2 to dilate vessels
48
Q

what type of receptor does noradrenaline have a higher affinity for and where does it act?

A
  • Noradrenaline has a higher affinity for α over β, mainly acts at α1 receptors to constrict vessels
49
Q

where does adrenaline cause vasoconstriction and vasodilation?

A 
most tissues (GI tract, skin etc.)
-vasoconstriction

skeletal muscle, coronary circulation
-vasodilation

50
Q

Effect of iv Adrenaline vs iv Noradrenaline on Circulation

A

NA

  • a1 skeletal muscle arteriole constriction, TPR increases
  • this increases BP, stimulating baroreceptors which therefore decrease HR slightly
  • drop in HR causes a decrease in CO

Adrenaline

  • b2 skeletal muscle arteriole vasodilation, TPR decreases which causes CO to increase (b1 receptors on heart)
  • BP doesn’t change much, good during exercise
51
Q

brief explain the Renin-Angiotensin-Aldosterone System (RAAS):

A
  • you become dehydrated and BP drops
  • low BP/Na triggers kidney to release renin, which cleaves off 10 amino acids from angiotensinogen - this decapetide is angiotensin I
  • Angiotensin I travels to the lungs where ACE cleaves off 2 amino acids to make an octapeptide called Angiotensin II
52
Q

what are the effects of angiotensin II?

A
  • central effects: increased sympathetic drive, thirst
  • vasoconstriction, increasing TPR and BP, and stimulating sympathetic nerves
  • adrenal glands stimulated to produce aldosterone, which retains more sodium from kidneys ( ie. more sodium brought back into blood).
  • increase in NaCl in blood increases osmotic potential of blood so fluid from interstitial space moves into blood
53
Q

what is the hypothalamus response stimulated by?

A

an increase in osmolarity

o i.e. dehydration or low blood volume

54
Q

what is ADH involved in?

A

the maintenance of BP

55
Q

how does ADH maintain BP?

A
  • ADH causes vasoconstriction

- ADH increases the renal absorption of water, so you lose less water

56
Q

where is ADH released from?

A

the posterior of the pituitary gland

57
Q

what are the regions of the brain involved in ADH release and how do they work?

A
  • Stretch receptors in the left atrium have continuous signals causing firing in the NTS
    o This sends out inhibitory nerves to the CVLM
  • The CVLM stimulates the pituitary to release vasopressin so stretching of the heart inhibits this
  • Dehydration or haemorrhage NTs inhibition is switched off and CVLM stimulates vasopressin
    o NTS is the thermostat that sets the level at which the CVLM is inhibited
58
Q

what does NTS do?

A

inhibit CVLM

59
Q

what is the role of CVLM?

A

CVLM stimulates ADH release

60
Q

what is Atrial Natriuretic Peptide (ANP) released by, and when is it released?

A

specialised atrial myocytes (when the blood volume is too high)

61
Q

where does ANP act and what does it do?

A
  • acts at ANP receptors on vascular smooth muscle cells, especially in the arteries going towards the glomerulus
  • increases the cGMP pathway (like NO)
  • causes systemic vasodilation (increasing GFR), opposing the action of noradrenaline, RAAS, ADH
62
Q

what is the effect of the dilatation of renal afferent arterioles?

A

GFR is increased

63
Q

what is the effect of ANP dilating blood vessels

A

-Dilatation of renal afferent arteriole increases GFR

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

sem 2 CVS (17 decks)

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