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CVPR > CVPR Week 4: Vascular smooth muscle and endothelial cells > Flashcards

CVPR Week 4: Vascular smooth muscle and endothelial cells Flashcards

1
Q

Application of ACh to vasculature will provoke this response

A

Dilation

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2
Q

What are the primary resistance vessels?

A

Arterioles

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3
Q

Arteriole function related to ‘primary resistance vessels’

2 listed

A
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4
Q

Identify

A
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5
Q

Identify + role of intrinsic and extrinsic factors

A
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6
Q

How is vascular tone mediated?

A

through smooth muscle contraction/relaxation

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7
Q

How is vascular tone regulated?

A
  • Contraction can be initiated by chemical or electrical signals or both
  • through intrinsic/extrinsic factors
  • Sympathetic innervation
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8
Q

Spatial control of vasculature: Sympathetic nerves

A

effects the vasculature throughout the whole body

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9
Q

Spatial control of vasculature: Extrinsic factors

A

effects the vasculature throughout the whole body

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10
Q

Spatial control of vasculature: Intrinsic factors

A

Have a regional effect on vasculature

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11
Q

Examples of extrinisic factors of vascular control

A

Neurohumoral (i.e sympathetic activation)

circulating factors (i.e. hormones)

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12
Q

Neurohumoral activation description

A

refers to increased activity of the sympathetic nervous system, renin-angiotensin system, vasopressin and atrial natriuretic peptide.

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13
Q

Examples of intrinisic factors of vascular control

3 listed

A
  • endothelial factors
  • mechanical factors (i.e. flow and pressure)
  • metabolites
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14
Q

Sympathetic activation of the vasculature

A

NE or EPI released and bound by α and β receptors causing smooth muscle contraction or dilation

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15
Q

EPI affinity deficit

A

EPI has a higher affinity for β2 receptor over α1 which would result in vasodilation over vasoconstriction

Low amounts of epi stimulate β2 over α1

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16
Q

Sympathetic activation of α1 receptors causes smooth muscle contraction in?

6 listed

A
  • vasculature (all systemic vessels)
  • eye
  • bladder
  • prostate
  • uterus

However, in the GI tract α1 receptors causes relaxation

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17
Q

Stimulation of α1 receptors in this location causes relaxation

A

GI tract

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18
Q

Stimulation of α1 receptors in the GI tract causes?

A

smooth muscle relaxation

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19
Q

Sympathetic activation of β2 receptors causes

A

vasodilation (in vessels supplying skeletal muscle, liver and heart)

and relaxation of

  • Eye
  • Bronchioles
  • Bladder
  • Uterus
  • GI Tract
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20
Q

At low concentrations of EPI you will see what response in the vasculature?

A

Vasodilation

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21
Q

At high concentrations of EPI you will see what response in the vasculature?

A

Vasoconstriction (due to the increased activation of α1 receptors

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22
Q

Objectives

A
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23
Q

Identify

A
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24
Q

Excitation-contraction coupling in skeletal muscle

A

electrical volatage causes confirmational change in the Dihydropyridine receptor which is physically inked to the ryanodine receptor which opens the ryandoine receptor and releases from the sarcoplasmic reticulum

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25
Q

Excitation-contraction coupling in cardiac muscle

A
  • Calcium-induced calcium release through the stimulation of L-type voltage-gated Ca2+ channel (L-type VGCCs) through an SA nodal action potential and Ca2+ is brought into the cell and activates the Ryanodine receptor which is not physically linked to release more Ca2+ from the Sarcoplasmic reticulum
  • Can be modulated by EPI or NE through (Gs coupled receptors) linked to adenylate cyclase which stimulate it to increase cAMP to further increase CICR from the SR and voltage-gated Ca2+ receptors in the cell membrane and increasing HR and contractility
  • Can also be modulated by ACh through Gi coupled receptors which inhibit adenylate cyclase and decrease Ca2+ release thereby decreasing cAMP, HR and contractility
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26
Q

Explain the differences in excitation-contraction coupling in skeletal muscle versus cardiac muscle

A
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27
Q

Excitation-contraction coupling in smooth muscle

A
  • Similar to cardiac muscle through the use of voltage-dated Ca 2+ L-type Channels (VGCCs L-type) opening as a result of an action potential and stimulation of non-physically linked ryanodine receptor to release Ca2+ from the sarcoplasmic reticulum

However, the main difference is through receptor coupling in the form of PlP2 Gq coupled noradrenergic (α 1) receptors which are activated by NE and EPI and take Phospholipase C into DAG and IP3

  • IP3 channels also further increase Ca2+ release
  • So you have ryanodine receptors as well as IP3Rs on the SR
  • And activation of DAG results in the activation of PKC which stimulates opening of ROC channels (Receptor-operated channels) which are non-selective for Na+/Ca2+, where the Ca2+ contributes further to CICR and the Na+ further contributes to membrane depolarization
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28
Q

Gq PCR agonists

6 listed

A
  • NE/EPI
  • Endothelin 1
  • Thromboxane A2
  • Vasopressin
  • ACh
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29
Q

NE/EPI Gq PCR

A

α1 noradrenergic receptor

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30
Q

Angiotensin II Gq PCR

A

AT1

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31
Q

Endothelin I Gq PCR

2 listed

A

ETA/ETB

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32
Q

Thromboxane A2 Gq PCR

A

TXA2R

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33
Q

Vasopressin Gq PCR

A

V1

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34
Q

ACh Gq PCR

A

M3

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35
Q

ACh Gq PCR location

A

on non-vascular smooth muscle cells

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36
Q

Smooth muscle cells closing of K+ channels

A

will lead to depolarization of the cell

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37
Q

Similarities of actomyosin regulation of smooth and striated muscle cells

A
  • Ca2+ is important for contraction
  • Force is created by an actin-myosin crossbridge interaction between sliding filaments
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38
Q

Differences of actomyosin regulation of smooth and striated muscle cells

A
  • the organization of actin-myosin filaments
  • Ca2+ regulation of contraction
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39
Q

What gives rise to the striated appearance in skeletal and cardiac muscle?

A

the sarcomere functional unit

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40
Q

Sarcomere structural-functional relationship

2 listed

A
  • contraction occurs in one direction
  • limits the force and velocity of contraction
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41
Q

Sarcomeres in smooth muscle cellls

A

Smooth muscle cells lack sarcomeres

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42
Q

Identify

A
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43
Q

Contractile unit in smooth muscle cells

A
  • Actin filaments are attached to dense bodies
  • myosin filaments aren’t attached to anything but actin
  • The actin-myosin contractile units are arranged in different directions
  • can rearrange very rapidly
  • maintain same amount of force on contraction but are added in series or parallel
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44
Q

Ca2+ in striated muscle

A
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45
Q

Smooth muscle Troponin

A
  • smooth muscle cells don’t have troponin inhibiting actin

Instead,

  • Ca2+ binds to calmodulin and this complex activates myosin like chain kinase (MLCK)
  • MLCK phosphorylates myosin head and allows for contraction
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46
Q

Skeletal muscle contraction is dependent on?

A

Ca2+

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47
Q

Smooth muscle contraction is dependent on?

A

MLCK phosphorylation of the myosin head

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48
Q

In smooth muscle how is relaxation mediated?

6 listed

A
  • MLCP (phosphatase) dephosphorylates the myosin head
  • decrease cytosolic [Ca2+]
  • open K+ leak channels to hyperpolarize the cell
  • Inhibit MLCK
  • cAMP
  • cGMP
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49
Q

Cyclic molecules and smooth muscle

A

cAMP inhibits MLCK and reduce intracellular [Ca2+]

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50
Q

cAMP is produced by what interaction in smooth muscle

A
  • EPI
  • Prostacyclin
  • Adenosine

Through Gs coupled receptors

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51
Q

cAMP effect on smooth muscle

A

inhibits MLCK and thereby reducing [Ca2+] inside the smooth muscle cell

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52
Q

cGMP effect on smooth muscle cells

A
  • Activates MLCP thereby reducing intracellular [Ca2+]
  • as well as other mechanisms of reducing [Ca2+] inside the cell
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53
Q

NO effect on GTP

A

converts GMP into cGMP through activation of sGC (soluble guanylyl cyclase)

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54
Q

Major stimulus converting GTP into cGMP in smooth muscle

A

NO (nitric oxide)

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55
Q

Particulate guanylyl cyclase description

A

instead of soluble in the cell is on the membrane and is activated by atrial natriuretic and brain natriuretic peptides

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56
Q

Particulate guanylyl cyclase is activated by?

A

activated by atrial natriuretic and brain natriuretic peptides

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57
Q

ANP AKA

A

Atrial natriuretic peptide

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58
Q

BNP AKA

A

Brain natriuretic peptide

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59
Q

Net effect of ANP and BMP on smooth muscle

60
Q

cAMP in smooth and cardiac muscle cells

A

causes relaxation in the vasculature and smooth muscle cells by inhibiting MLCK which is necessary for contraction

In cardiac cells cAMP is activating L-type VGCCs which is stimulatory toward contraction (increase HR and contractility)

61
Q

Smooth muscle cells are well-suited for

A

tonic contraction (partial contraction)

62
Q

Smooth muscle cell contraction speed

A
  • slower than skeletal and cardiac muscle
63
Q

Smooth muscle energy usage

A

use much less energy for the amount of force generated and maintained

64
Q

Smooth muscle endurance

A

can sustain contractions for very long periods without becoming fatigued

65
Q

Smooth muscle contraction is regulated by?

A

the phosphorylation of the myosin head

66
Q

Smooth muscle contraction and membrane potential

A

contraction is not always associated with changes in membrane potential

67
Q

Smooth muscle contractile unit arrangement

A

not arranged in sarcomeres which is an important feature which allows smooth muscle cells to undergo rearrangement with a constant force of contraction

68
Q

Smooth muscle contraction and Ca2+s role

A

smooth muscle cells do not have troponin and use Ca2+ to regulate MLCK activation so it is indirectly linked to cross-bridge cycling by whether or not myosin is phosphorylated

69
Q

Endothelial cell description

A
  • is highly metabolically active
  • is considered an organ
  • with important endocrine and autocrine function that affect both underlying smooth muscle cells and other cells in the blood
70
Q

Endothelial cell function

5 listed

A
  • involved in leukocyte trafficking and inflammation
  • involved in hemostasis
  • serves in barrier function and permeability
  • involved in smooth muscle cell homeostasis (keeps them quiescent and prevents unnecessary proliferation)
  • involved in vascular tone and blood flow
71
Q

Why do Endothelial cells need Ca2+ ?

A
  • needed to produce the vasoactive products that are generated in the endothelium
72
Q

Stimuli for Ca2+ change in endothelial cells

A
  • mechanical stress (shear stress of laminar flow)
  • Receptor activation (Gq coupled receptors)
73
Q

Endothelial cells Ca2+ release mechanisms

A
  • don’t have ryanodine receptors like muscle cells to stimulate release of Ca2+ from intracellular stores
  • intracellular store release is through IP3 receptors
  • don’t have VGCCs just have ROCs
74
Q

ACh effect on smooth muscle

A

causes contraction of smooth muscle

75
Q

ACh effect on eye

A

constricts the pupil (sphincter pupilae)

76
Q

ACh effect on lungs

A

constrict bronchioles and increases secretion

77
Q

ACh effect on heart

A

decreased HR

78
Q

ACh effect on blood vessels

A

M3 not on the smooth muscle cells but on the endothelial cells

dilates (through release of NO)

79
Q

ACh effect on GI

A
  • increases peristalsis
  • increases secretions
80
Q

ACh effect on bladder

A

contraction for micturation

81
Q

ACh effect on salivary glands

A

increased salivation

82
Q

NO is produced where?

A
  • by endothelial cells
  • by endothelial nitric oxide synthase
83
Q

endothelial nitric oxide synthase reaction

A

uses Oxygen and a cofactor to produce NO

converts L-arginine to L citrulline

84
Q

Drugs that take advantage of NO’s dilation of the vasculature

A

want to increase NO production leading to the relaxation of vascular smooth muscle cells

  • Arginase inhibitor to keep more substrate around

Directly stimulate vascular smooth muscle cells

  • Inhaled NO
  • Nitrates - nitroglycerin (angina) reduces hypoxia and helps blood flow in coronary vessels
  • sGC activators
  • inhibit PDE5 (prevents the breakdown of cGMP into GMP) VIAGRA!!!
85
Q

Metabolites of arachidonic acid vasoactive metabolites

A
  • Thromboxane A2
  • prostacyclin (PGl2)
86
Q

main Vasoactive metabolites of arachidonic acid

2 listed

A
  • Thromboxane A2
  • prostacyclin (PGl2)
87
Q

Vasoactive metabolites of arachidonic acid activation mechanisms

A
  • shear stress from laminar flow
  • receptor activation (Ca2+ causes the activation of phospholipase A2 which releases stored arachidonic acid which was stored in membrane phospholipids
  • once released can be metabolized into other active compounds (enzyme such as COX-1 and COX-2)
88
Q

Prostacyclin effect on the vasculature

A

relaxation (through Gs coupled receptor increasing cAMP)

89
Q

Thromboxane A2 effect on the vasculature

A

causes contraction (through Gq coupled PLC pathway)

90
Q

Targets of arachidonic acid metabolites

91
Q

Thromboxane A2 effect on platelets

A
  • vasoconstriction
  • platelet aggregation
  • Thrombosis
92
Q

Prostaglandins effect on gastric mucosa

93
Q

Prostaglandins effect on joints

94
Q

Prostacyclin effect on endothelial cells

A
  • Vasodilation
  • reduced platelet aggregation
95
Q

NSAIDs inhibit?

A

COX-1&2

to try to prevent pain and inflammation and fever

side effects causes gastric ulcers

96
Q

Corticosteroids inhibit

A

Phospholipase A2 (PLA2)

97
Q

Selective COX-2 inhibitors

A

celebrex

however, increased risk of cardiovascular disease because reduced vasodilation

98
Q

Know what COX inhibitors inhibit and what side effects they may have

99
Q

Prostacyclin analogues

100
Q

Endothelin-1 features

A

can act as a vasodilator or vasoconstrictor

101
Q

Endothelin-1 production

102
Q

Endothelin-1 paracrine autocrine

A

since there is a constant production of Endothelin-1 it can act as an autocrine factor

103
Q

Endothelin-1 storage

A

stored in vesicles in the endothelial cells

104
Q

Endothelin-1 function

A

can lead to production of NO and PGl2 leading to vascular relaxation and antihypertrophic effect on smooth muscle cells

105
Q

Endothelin-1 circulating levels

A

these receptors take up excess Endothelin-1 and clears circulating levels

106
Q

When there is a Endothelin-1 overproduction

A

Endothelin-1 acts in a paracrine fashion and binds directly to receptors on smooth muscle cells which will lead to contraction of smooth muscles (very potent vasoconstrictor when it reaches high levels, also proliferative as well)

107
Q

Endothelin-1 smooth muscle receptors

A

ETA and ETB

108
Q

Selective ETA and ETB inhibitors

109
Q

Angiotensin II description

A

a potent vasoconstrictor

110
Q

Angiotensin II production

A
  • Angiotensinogen produced in the liver and goes into circulation
  • converted to Angiotensin I by renin which is produced by the juxtaglomerular cells of the kidney
  • converted to angiotensin II by ACE enzyme
111
Q

ACE location & function

3 listed

A
  • ACE is lovated on the endothelial cells and Ang II leads to contraction
  • ACE breaks down bradykinin which could have caused vasodilation
  • so ACE contributes to contraction by Ang II and through breakdown of bradykinin
112
Q

ACE inhibitor function

A

inhibits ACE preventing

  • Angiotensin I conversion to Angiotensin II
  • the breakdown of bradykinin
113
Q

AT1 blocker function

A

blocks angiotensin II receptors preventing the vasoconstriction

114
Q

The important roles of endothelial factors

A

Prostacyclin & NO - anti-inflammatory and anti-thrombotic, NO is for relaxation Prostacyclin is antihypertrophic

Thromboxane and Endothelin-1 - pro-inflammatory and prothrombotic, ET1 is vasoconstriction, TXA2 is mitogenic causing remodeling of the vascular wall

115
Q

An important trigger for endothelial dysfunction

A

oxidative stress

116
Q

How does oxidative stress cause endothelial dysfunction?

A

all of these things shift the endothelium from producing healthy protective factors but it produces more of the harmful factors

117
Q

Onset of endothelial dysfunction

A

insidious onset over a long time

want to test early on for endothelial function

118
Q

Tests of endothelial function

4 listed

119
Q

Invasive tests of endothelial function

2 listed

120
Q

ACE location

A

ACE is loCated on the endothelial cells and Ang II leads to contraction

121
Q

ACE function

A

ACE breaks down bradykinin which could have caused vasodilation

122
Q

ACE Effects

A

ACE contributes to vascular smooth muscle contraction by Ang II and through the breakdown of bradykinin

123
Q

Non-Invasive tests of endothelial function

2 listed

124
Q

Endothelial dysfunction results in?

A

reduced responsiveness to ACh and prevents dilation like they shoud

125
Q

Treatments of endothelial dysfunction

5 listed

A
  • diet and exercise (REALLY GOOD)
  • ACE
  • nitrate therapy
  • lipid-lowering drugs
  • alpha-beta blockers
126
Q

Vascular sensitivity to atherosclerotic lesions

A
  • occur at curves or bifurcations because of the disturbed flow causing decreased expression of COX-2 and ENOS (produces NO)
  • so these areas are more prone
  • shows how shear stress is very important for a function endothelium
127
Q

Role of endothelial cells in angiogensis

128
Q

Vasculogenesis description

A

occurs from progenitor cells

129
Q

Angiogenesis description

A

formation of new blood vessels from existing blood vessels

130
Q

Normal angiogenesis causes

4 listed

A
  • wound healing
  • muscle mass increase
  • acclimation to altitude
  • pregnancy fetal supply
131
Q

Pathogenic angiogenesis causes

A
  • cancer
  • stroke
  • diabetes
  • obesity
  • heart disease
  • multiple sclerosis
  • Alzheimer’s DIsease
  • Retinopathy
  • Preeclampsia
132
Q

Blood vessel growth regulation

A
  • Hypoxia is a huge stimulus for the production of angiogenic growth factors
  • however other things can too such as diabetes, retinopathy, cancer, etc
133
Q

Cause of insufficient angiogenesis

3 listed

A
  • Age
  • low VEGF
  • H. Pylori
134
Q

refraction of the vasculature AKA

A

pruning of the vasculature

135
Q

The most important mediator of angiogenesis

136
Q

Process of angiogenesis look over

A
  • bind to receptors on endothelial cells
  • migrate towards the source of VEGF
  • HDL4 and NOTCH
  • platelets come in through platelet-derived growth factor
137
Q

Cells that initiate angiogenesis

A

Endothelial cells

138
Q

Anti-VEGF therapies use

A

commonly used in cancer and other morbidities

139
Q

Consequences of anti-VEGF therapy

A
  • decreased vasodilator production NO PGl2
  • increased vasoconstrictors
  • microvascular refraction
  • ROS oxidative stress
  • Pressure naturesis
  • decreased lymphangiogenesis
  • all leads to vascular remodeling and increased peripheral resistance and volume overload
  • 80-100% of patients on these therapies get hypertension and cardiovascular disease
140
Q

Summary of angiogenesis

141
Q

Question 1

142
Q

Question 2

143
Q

Question 3

144
Q

Question 4

145
Q

Question 5

146
Q

Question 6

CVPR (93 decks)

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