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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
TISSUE METABOLITE vasodilators (4)
CO2 Lactate H+ Adenosine
26
TISSUE METABOLITE vasoconstrictor
O2
27
SNS plays an important part in controlling which factor of the CV system
TPR
28
What BVs are NOT by the SNS
Capillaries and small arterioles
29
What does innervation of larger arterioles allow
Sympathetic stimulation to increase resistance =\> blood flow decreases to an organ
30
sympathetic stimulation of veins results in
Change in volume of blood contained in vessels =\> changes venous return and CO
31
Where is there dense sympathetic innervation of arterioles
- skin - kidney - gut
32
Where is there poor innervation of arterioles
- brain - heart
33
Name given to when there is constant firing of SNS
Resting vasomotor tone
34
When are vasodilator metabolites produced What is the response
Whenever supply of O2 falls below O2 consumption decrease in local vascular resistance increase in blood flow to meet tissue needs
35
What does an increase in blood flow cause (regarding metabolites)
Causes a washout of metabolite - increase in resistance - decrease in blood flow
36
Where are adrenaline and epinephrine released
From adrenal medulla
37
What does noradrenaline always cause
Vasoconstriction
38
What is the action of adrenaline proportional to
Relative distribution of alpha-adrenergic and beta-adrenergic receptors in vasculature of organ
39
What organs have high beta-adrenergic receptor density
Heart vasculature Skeletal muscle vasculature =\> vasodilation // adrenaline
40
name 2 vasoconstrictors
Ang II - powerful ADH
41
What sort of resistance do gap junctions have
Low resistance
42
What is the arrangement of the actin and myosin filaments like
Irregular
43
How are thin, long actin filaments anchored to the cell membrane
They are binded to dense bodies
44
What leads to SM relaxation
De-phosphorylation of MLCK
45
What happens when actin and myosin continue to interact What is maintained as a result
Latch-bridges form, which either do not detach or detach slowly A level of tension is maintained with little consumption of ATP
46
What is the RMP of most SM cells
-50 -\> -60 mV, which is 30 mV more +ve than K+ equilibrium potential
47
2 points about the flow of ions across cell membrane of SM
1. Outward K+ I 2. Inward Ca2+ I - leak channels =\> constant state of partial contraction
48
What does the constant state of partial contraction of VSM cells generate
Sustained BASAL TONE Some arterioles are partially constricted from birth -\> death
49
How do vasoconstrictors constrict BVs
By increasing active tension in VSM cells
50
Name the 2 mechanisms for vasoconstriction Which NT works with both mechanisms
1. Stretch-operated channels - RAPID 2. IP3. mechanism - SUSTAINED Noradrenaline
51
3 hormones involved in vasoconstriction
Adrenaline Ang II Endothelin I
52
Explain the IP3 mechanism
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
How do vasodilators dilate BVs
By decreasing active tension in VSM cells By decreasing IC [Ca2+]i
54
Effect of hyperpolarisation on VG Ca2+ channels
Decrease probability that VG Ca2+ channels will open
55
What is hyperpolarisation mediated by
Activation of K+ channels * decrease in [Ca2+]i * Relaxation of VSm * BV dilates
56
Effect and mechanism of action of adrenaline in arterioles
VASODILATION B2-adrenoreceptors - binds to G proteins - skeletal muscle - heart
57
What does G protein activate
Adenylate cyclase - increase IC [cAMP]
58
1st step in cAMP mediated vasodilation
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
2nd step in cAMP-mediated vasodilation
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
What happens when histamine binds to its H1 receptor
Induces vasodilation by the cAMP-mediated mechanism
61
What does the presence of endothelium result in
Release of vasodilator substance - EDRF or NO
62
What does the absence of endothelium result in
ACh causes VSM cells to contract - BVs contract
63
What are laminae
Thin concentric shells that fluid behaves as as it moves through a small cylindrical tube at moderate velocity
64
What do the laminae in contact with vessel wall have
0 velocity due to cohesive forces =\> zero-sup condition
65
Outer lamina resistance
Outer lamina slide with greater ease and therefore velocity =\> blood in the centre of the vessel has highest velocity
66
What is the velocity profile in a BV
PARABOLIC
67
What does shear mean
Sliding motion of 1 lamina past another
68
What does shear cause
RBCs to migrate away from vessel wall
69
What is shear stress What does shear stress increase with
Friction between molecules in adjacent laminae exerts a dragging force on its neighbour Increases with rate of sliding and fluid viscosity
70
What does shear stress do at vessel wall
Tugs on glycocalyx (polymer coating rooted in endothelium)
71
What does this shear stress stimulate
Endothelium to secrete regulatory vasoactive agents e.g. NO

CV physiology (from notes) (10 decks)

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