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CV physiology (from notes) > Vascular SM, BVs and Vasodilation/Vasoconstriction > Flashcards

Vascular SM, BVs and Vasodilation/Vasoconstriction Flashcards

1
Q

Where is pulsatility lost

A

In arterioles

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2
Q

Where is there a major site of pressure fall

A

In arterioles 75 mmHg -> 35 mmHg

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3
Q

Where is there a further pressure fall

A

Capillaries 35 mmHg -> 15 mmHg

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4
Q

What is the pressure gradient driving blood back to the heart through veins like

A

It’s LOW

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5
Q

Relationship between pressure and flow

A

V = I x R MAP = CO x TPR R = change in pressure/flow (CO)

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6
Q

Importance of the site of the biggest pressure drop

A

MAJOR SITE OF RESISTANCE => arterioles

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7
Q

Poiseuille’s Law

A

R = 8 x n x l/pi x r4

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8
Q

What is a major determinant of blood viscosity (n)

A

Hct decreased Hct in anaemia => decreased resistance to flow Increased Hct in polycythemia => increased resistance to flow

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9
Q

Radius of vessel and resistance

A

R is proportional to 1/r4

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10
Q

How are resistances arranged MOSTLY in systemic circulation

A

in parallel

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11
Q

What is autoregulation

A

When metabolism with an organ is constant, autoregulation keeps blood flow constant in the face of changing arterial BP

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12
Q

What is the critical closing pressure

A
  • Flow drops to 0 at a pressure of 20-30 mmHg
  • This critical closing pressure is believed to be the minimum pressure necessary to keep small blood vessels open
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13
Q

Pressure range where blood flow is constant

A

70 -170 mmHg

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14
Q

What is the myogenic response

A

Originates in SM cells

SM cells contract in response to increase in arterial wall tension when BP rises

SM cells relax in responsr to decrease in arterial wall tension when BP falls

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15
Q

Mechanism of action for myogenic response

A
  1. Increase stretch of VSM
  2. Spread of depolarisation through gap junctions
  3. VSM cell opens stretch-operated Ca2+ channels and allows more Ca2+ into cell
  4. => increased force of contraction
  5. Increased resistance

NT = noradrenaline

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16
Q

What factor is important in maintenance of BP

A

TPR

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17
Q

What would happen if the arterioles were to dilate simultaneously

A

BP would drop to a dangerously low level

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18
Q

4 factors influencing tension/tone of vascular SM

A
  1. Local factors
  2. Neural activity
  3. Hormones
  4. Paracrines
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19
Q

Structure of VSM cells

A
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20
Q

Neural activity - impact on tone of VSM

A

sympathetic activity - neurogenic

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21
Q

What are HORMONAL vasoconstrictors

A
  • Epinephrine acting on alpha-receptors
  • ADH
  • Ang II
  • Cortisol
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22
Q

What are HORMONAL vasodilators

A

Epinephrine acting on beta-receptors

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23
Q

PARACRINE vasoconstrictors (2)

A

Some prostaglandins (endothelium and platelets)

EDCF (endothelin)

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24
Q

PARACRINE vasodilators (3)

A

Some prostaglandins (including prostacyclin)

Histamine

EDRF (NO)

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25
Q

TISSUE METABOLITE vasodilators (4)

A

CO2

Lactate

H+

Adenosine

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26
Q

TISSUE METABOLITE vasoconstrictor

A

O2

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27
Q

SNS plays an important part in controlling which factor of the CV system

A

TPR

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28
Q

What BVs are NOT by the SNS

A

Capillaries and small arterioles

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29
Q

What does innervation of larger arterioles allow

A

Sympathetic stimulation to increase resistance => blood flow decreases to an organ

30
Q

sympathetic stimulation of veins results in

A

Change in volume of blood contained in vessels

=> changes venous return and CO

31
Q

Where is there dense sympathetic innervation of arterioles

A
  • skin
  • kidney
  • gut
32
Q

Where is there poor innervation of arterioles

A
  • brain
  • heart
33
Q

Name given to when there is constant firing of SNS

A

Resting vasomotor tone

34
Q

When are vasodilator metabolites produced

What is the response

A

Whenever supply of O2 falls below O2 consumption

decrease in local vascular resistance

increase in blood flow to meet tissue needs

35
Q

What does an increase in blood flow cause (regarding metabolites)

A

Causes a washout of metabolite

  • increase in resistance
  • decrease in blood flow
36
Q

Where are adrenaline and epinephrine released

A

From adrenal medulla

37
Q

What does noradrenaline always cause

A

Vasoconstriction

38
Q

What is the action of adrenaline proportional to

A

Relative distribution of alpha-adrenergic and beta-adrenergic receptors in vasculature of organ

39
Q

What organs have high beta-adrenergic receptor density

A

Heart vasculature

Skeletal muscle vasculature

=> vasodilation // adrenaline

40
Q

name 2 vasoconstrictors

A

Ang II - powerful

ADH

41
Q

What sort of resistance do gap junctions have

A

Low resistance

42
Q

What is the arrangement of the actin and myosin filaments like

43
Q

How are thin, long actin filaments anchored to the cell membrane

A

They are binded to dense bodies

44
Q

What leads to SM relaxation

A

De-phosphorylation of MLCK

45
Q

What happens when actin and myosin continue to interact

What is maintained as a result

A

Latch-bridges form, which either do not detach or detach slowly

A level of tension is maintained with little consumption of ATP

46
Q

What is the RMP of most SM cells

A

-50 -> -60 mV, which is 30 mV more +ve than K+ equilibrium potential

47
Q

2 points about the flow of ions across cell membrane of SM

A
  1. Outward K+ I
  2. Inward Ca2+ I - leak channels => constant state of partial contraction
48
Q

What does the constant state of partial contraction of VSM cells generate

A

Sustained BASAL TONE

Some arterioles are partially constricted from birth -> death

49
Q

How do vasoconstrictors constrict BVs

A

By increasing active tension in VSM cells

50
Q

Name the 2 mechanisms for vasoconstriction

Which NT works with both mechanisms

A
  1. Stretch-operated channels - RAPID
  2. IP3. mechanism - SUSTAINED

Noradrenaline

51
Q

3 hormones involved in vasoconstriction

A

Adrenaline

Ang II

Endothelin I

52
Q

Explain the IP3 mechanism

A
  1. Binding of agent to receptor activates PLC
  2. PLC catalyses breakdown of PIP2 -> IP3 (inositol triphosphate)
  3. IP3 stimulates release of Ca2+ from SR
53
Q

How do vasodilators dilate BVs

A

By decreasing active tension in VSM cells

By decreasing IC [Ca2+]i

54
Q

Effect of hyperpolarisation on VG Ca2+ channels

A

Decrease probability that VG Ca2+ channels will open

55
Q

What is hyperpolarisation mediated by

A

Activation of K+ channels

  • decrease in [Ca2+]i
  • Relaxation of VSm
  • BV dilates
56
Q

Effect and mechanism of action of adrenaline in arterioles

A

VASODILATION

B2-adrenoreceptors - binds to G proteins

  • skeletal muscle
  • heart
57
Q

What does G protein activate

A

Adenylate cyclase

  • increase IC [cAMP]
58
Q

1st step in cAMP mediated vasodilation

A

PHOSPHORYLATION OF Ca2+-ATPase PUMPS

  • cAMP activates protein kinase A
  • PKA P Ca2+-ATPase pump on cell membrane => Ca2+ extrusion increases
  • PKA P PHOSPHOLAMBAN on SR - Ca2+ re-uptake // SR increases
  • [Ca2+]i decreases and VSM relaxes
59
Q

2nd step in cAMP-mediated vasodilation

A

PHOSPHORYLATION OF K+ CHANNELS

  • PKA P K+ channels - K+ leaving the cell => HYPERPOLARISATION
  • More -ve MP closes VG Ca2+ channel
  • Decreased Ca2+ entry => decreased [Ca2+]i
  • VSM relaxation occurs
60
Q

What happens when histamine binds to its H1 receptor

A

Induces vasodilation by the cAMP-mediated mechanism

61
Q

What does the presence of endothelium result in

A

Release of vasodilator substance - EDRF or NO

62
Q

What does the absence of endothelium result in

A

ACh causes VSM cells to contract - BVs contract

63
Q

What are laminae

A

Thin concentric shells that fluid behaves as as it moves through a small cylindrical tube at moderate velocity

64
Q

What do the laminae in contact with vessel wall have

A

0 velocity due to cohesive forces => zero-sup condition

65
Q

Outer lamina resistance

A

Outer lamina slide with greater ease and therefore velocity => blood in the centre of the vessel has highest velocity

66
Q

What is the velocity profile in a BV

67
Q

What does shear mean

A

Sliding motion of 1 lamina past another

68
Q

What does shear cause

A

RBCs to migrate away from vessel wall

69
Q

What is shear stress

What does shear stress increase with

A

Friction between molecules in adjacent laminae exerts a dragging force on its neighbour

Increases with rate of sliding and fluid viscosity

70
Q

What does shear stress do at vessel wall

A

Tugs on glycocalyx (polymer coating rooted in endothelium)

71
Q

What does this shear stress stimulate

A

Endothelium to secrete regulatory vasoactive agents e.g. NO

CV physiology (from notes) (10 decks)

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