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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
Excitation-contraction coupling in cardiac muscle
* 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
26
Explain the differences in excitation-contraction coupling in skeletal muscle versus cardiac muscle
27
Excitation-contraction coupling in smooth muscle
* 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
28
Gq PCR agonists 6 listed
* NE/EPI * Endothelin 1 * Thromboxane A2 * Vasopressin * ACh
29
NE/EPI Gq PCR
α1 noradrenergic receptor
30
Angiotensin II Gq PCR
AT1
31
Endothelin I Gq PCR 2 listed
ETA/ETB
32
Thromboxane A2 Gq PCR
TXA2R
33
Vasopressin Gq PCR
V1
34
ACh Gq PCR
M3
35
ACh Gq PCR location
on non-vascular smooth muscle cells
36
Smooth muscle cells closing of K+ channels
will lead to depolarization of the cell
37
Similarities of actomyosin regulation of smooth and striated muscle cells
* Ca2+ is important for contraction * Force is created by an actin-myosin crossbridge interaction between sliding filaments
38
Differences of actomyosin regulation of smooth and striated muscle cells
* the organization of actin-myosin filaments * Ca2+ regulation of contraction
39
What gives rise to the striated appearance in skeletal and cardiac muscle?
the sarcomere functional unit
40
Sarcomere structural-functional relationship 2 listed
* contraction occurs in one direction * limits the force and velocity of contraction
41
Sarcomeres in smooth muscle cellls
Smooth muscle cells lack sarcomeres
42
Identify
43
Contractile unit in smooth muscle cells
* 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
44
Ca2+ in striated muscle
45
Smooth muscle Troponin
* 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
46
Skeletal muscle contraction is dependent on?
Ca2+
47
Smooth muscle contraction is dependent on?
MLCK phosphorylation of the myosin head
48
In smooth muscle how is relaxation mediated? 6 listed
* MLCP (phosphatase) dephosphorylates the myosin head * decrease cytosolic [Ca2+] * open K+ leak channels to hyperpolarize the cell * Inhibit MLCK * cAMP * cGMP
49
Cyclic molecules and smooth muscle
cAMP inhibits MLCK and reduce intracellular [Ca2+]
50
cAMP is produced by what interaction in smooth muscle
* EPI * Prostacyclin * Adenosine Through Gs coupled receptors
51
cAMP effect on smooth muscle
inhibits MLCK and thereby reducing [Ca2+] inside the smooth muscle cell
52
cGMP effect on smooth muscle cells
* Activates MLCP thereby reducing intracellular [Ca2+] * as well as other mechanisms of reducing [Ca2+] inside the cell
53
NO effect on GTP
converts GMP into cGMP through activation of sGC (soluble guanylyl cyclase)
54
Major stimulus converting GTP into cGMP in smooth muscle
NO (nitric oxide)
55
Particulate guanylyl cyclase description
instead of soluble in the cell is on the membrane and is activated by atrial natriuretic and brain natriuretic peptides
56
Particulate guanylyl cyclase is activated by?
activated by atrial natriuretic and brain natriuretic peptides
57
ANP AKA
Atrial natriuretic peptide
58
BNP AKA
Brain natriuretic peptide
59
Net effect of ANP and BMP on smooth muscle
Dilation
60
cAMP in smooth and cardiac muscle cells
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
Smooth muscle cells are well-suited for
tonic contraction (partial contraction)
62
Smooth muscle cell contraction speed
* slower than skeletal and cardiac muscle
63
Smooth muscle energy usage
use much less energy for the amount of force generated and maintained
64
Smooth muscle endurance
can sustain contractions for very long periods without becoming fatigued
65
Smooth muscle contraction is regulated by?
the phosphorylation of the myosin head
66
Smooth muscle contraction and membrane potential
contraction is not always associated with changes in membrane potential
67
Smooth muscle contractile unit arrangement
not arranged in sarcomeres which is an important feature which allows smooth muscle cells to undergo rearrangement with a constant force of contraction
68
Smooth muscle contraction and Ca2+s role
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
Endothelial cell description
* 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
Endothelial cell function 5 listed
* 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
Why do Endothelial cells need Ca2+ ?
* needed to produce the vasoactive products that are generated in the endothelium
72
Stimuli for Ca2+ change in endothelial cells
* mechanical stress (shear stress of laminar flow) * Receptor activation (Gq coupled receptors)
73
Endothelial cells Ca2+ release mechanisms
* 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
ACh effect on smooth muscle
causes contraction of smooth muscle
75
ACh effect on eye
constricts the pupil (sphincter pupilae)
76
ACh effect on lungs
constrict bronchioles and increases secretion
77
ACh effect on heart
decreased HR
78
ACh effect on blood vessels
M3 not on the smooth muscle cells but on the endothelial cells dilates (through release of NO)
79
ACh effect on GI
* increases peristalsis * increases secretions
80
ACh effect on bladder
contraction for micturation
81
ACh effect on salivary glands
increased salivation
82
NO is produced where?
* by endothelial cells * by endothelial nitric oxide synthase
83
endothelial nitric oxide synthase reaction
uses Oxygen and a cofactor to produce NO converts L-arginine to L citrulline
84
Drugs that take advantage of NO's dilation of the vasculature
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
Metabolites of arachidonic acid vasoactive metabolites
* Thromboxane A2 * prostacyclin (PGl2)
86
main Vasoactive metabolites of arachidonic acid 2 listed
* Thromboxane A2 * prostacyclin (PGl2)
87
Vasoactive metabolites of arachidonic acid activation mechanisms
* 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
Prostacyclin effect on the vasculature
relaxation (through Gs coupled receptor increasing cAMP)
89
Thromboxane A2 effect on the vasculature
causes contraction (through Gq coupled PLC pathway)
90
Targets of arachidonic acid metabolites
91
Thromboxane A2 effect on platelets
* vasoconstriction * platelet aggregation * Thrombosis
92
Prostaglandins effect on gastric mucosa
93
Prostaglandins effect on joints
94
Prostacyclin effect on endothelial cells
* Vasodilation * reduced platelet aggregation
95
NSAIDs inhibit?
COX-1&2 to try to prevent pain and inflammation and fever side effects causes gastric ulcers
96
Corticosteroids inhibit
Phospholipase A2 (PLA2)
97
Selective COX-2 inhibitors
celebrex however, increased risk of cardiovascular disease because reduced vasodilation
98
Know what COX inhibitors inhibit and what side effects they may have
99
Prostacyclin analogues
100
Endothelin-1 features
can act as a vasodilator or vasoconstrictor
101
Endothelin-1 production
102
Endothelin-1 paracrine autocrine
since there is a constant production of Endothelin-1 it can act as an autocrine factor
103
Endothelin-1 storage
stored in vesicles in the endothelial cells
104
Endothelin-1 function
can lead to production of NO and PGl2 leading to vascular relaxation and antihypertrophic effect on smooth muscle cells
105
Endothelin-1 circulating levels
these receptors take up excess Endothelin-1 and clears circulating levels
106
When there is a Endothelin-1 overproduction
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
Endothelin-1 smooth muscle receptors
ETA and ETB
108
Selective ETA and ETB inhibitors
109
Angiotensin II description
a potent vasoconstrictor
110
Angiotensin II production
* 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
ACE location & function 3 listed
* 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
ACE inhibitor function
inhibits ACE preventing * Angiotensin I conversion to Angiotensin II * the breakdown of bradykinin
113
AT1 blocker function
blocks angiotensin II receptors preventing the vasoconstriction
114
The important roles of endothelial factors
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
An important trigger for endothelial dysfunction
oxidative stress
116
How does oxidative stress cause endothelial dysfunction?
all of these things shift the endothelium from producing healthy protective factors but it produces more of the harmful factors
117
Onset of endothelial dysfunction
insidious onset over a long time want to test early on for endothelial function
118
Tests of endothelial function 4 listed
119
Invasive tests of endothelial function 2 listed
120
ACE location
ACE is loCated on the endothelial cells and Ang II leads to contraction
121
ACE function
ACE breaks down bradykinin which could have caused vasodilation
122
ACE Effects
ACE contributes to vascular smooth muscle contraction by Ang II and through the breakdown of bradykinin
123
Non-Invasive tests of endothelial function 2 listed
124
Endothelial dysfunction results in?
reduced responsiveness to ACh and prevents dilation like they shoud
125
Treatments of endothelial dysfunction 5 listed
* diet and exercise (REALLY GOOD) * ACE * nitrate therapy * lipid-lowering drugs * alpha-beta blockers
126
Vascular sensitivity to atherosclerotic lesions
* 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
Role of endothelial cells in angiogensis
128
Vasculogenesis description
occurs from progenitor cells
129
Angiogenesis description
formation of new blood vessels from existing blood vessels
130
Normal angiogenesis causes 4 listed
* wound healing * muscle mass increase * acclimation to altitude * pregnancy fetal supply
131
Pathogenic angiogenesis causes
* cancer * stroke * diabetes * obesity * heart disease * multiple sclerosis * Alzheimer's DIsease * Retinopathy * Preeclampsia
132
Blood vessel growth regulation
* Hypoxia is a huge stimulus for the production of angiogenic growth factors * however other things can too such as diabetes, retinopathy, cancer, etc
133
Cause of insufficient angiogenesis 3 listed
* Age * low VEGF * H. Pylori
134
refraction of the vasculature AKA
pruning of the vasculature
135
The most important mediator of angiogenesis
VEGF
136
Process of angiogenesis look over
* bind to receptors on endothelial cells * migrate towards the source of VEGF * HDL4 and NOTCH * platelets come in through platelet-derived growth factor
137
Cells that initiate angiogenesis
Endothelial cells
138
Anti-VEGF therapies use
commonly used in cancer and other morbidities
139
Consequences of anti-VEGF therapy
* 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
Summary of angiogenesis
141
Question 1
142
Question 2
143
Question 3
144
Question 4
145
Question 5
146
Question 6

CVPR (93 decks)

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