Exam 3 Flashcards
1
Q
What does damage to endothelium by high lipids, smoking, hypertension, etc provoke?
A
A immune response
2
Q
What do immune cells become after they migrate under the endothelium?
A
Macrophages
3
Q
What do macrophages in the endothelium due to damage do?
A
Take up lipid and cholesterol, especially oxidized-LDL
4
Q
What is the next step in atherosclerosis after macrophage formation under the endothelium?
A
Smooth muscle cells migrate under endothelium and proliferate
5
Q
What do SMCs and immune cells become under the endothelium?
A
Lipid-laden foam cells
6
Q
What do lipid-laden foam cells form?
A
Fatty streak
7
Q
What forms over a fatty streak over time that is susceptible to being ruptured under trauma?
A
Fibrous plaques
8
Q
What happens to the fibrous plaques of atherosclerosis in advanced stages?
A
It becomes calcified with a core of dead cells
9
Q
What stage of atherosclerosis is most likely to be the most life threatening?
A
The fibrous plaque stage
10
Q
What is endothelial cell dysfunction mainly attributed to within the atherosclerotic process?
A
Decreased NO
11
Q
What do proper levels of NO do for the circulatory system?
A
1) Attenuate uptake of LDL and fibrinogen
2) Inhibit VCAM expression and leukocyte adhesion
3) Inhibit SMC Migration and proliferation
4) Inhibits platelet aggregation
12
Q
What type of effects does NO have?
A
Anti-atherogenic
13
Q
What effect does superoxide have on NO?
A
It combines to form peroxynitrite, thereby reducing the bioavailability of NO
14
Q
What does Peroxynitrite do?
A
- Uncouples eNOS by oxidizing its cofactor BH4
- This causes eNOS to make superoxide
15
Q
What effect does superoxide have on LDL?
A
It oxidizes LDL into its more atherogenic form
16
Q
What type of blood vessels usually grow with angiogenesis?
A
Venules
17
Q
What is arteriogenesis?
A
Growth and remodeling of pre-existing blood vessels
18
Q
Where does arteriogenesis usually happen?
A
Arteries and arterioles
19
Q
What is angiogenesis?
A
Growth of new blood vessels that sprout off of pre-existing vessels
20
Q
What are the steps of angiogenesis?
A
1) Hypoxia induces growth factor production (VEGF and FGF), angiogenic process begins in venules
2) Degradation of basal lamina by matrix metalloproteinases
3) Vacuolization of extending endothelial cells (This forms the new vessel lumen)
4) Proliferation of EC’s
5) Recruitment of pericytes that develop in SMC
21
Q
What happens to permeability in vessels as they age?
A
Hyper permeable when new, much less permeable as they develop
22
Q
What antiangiogenic factors keep angiogenesis in check?
A
Thrombospondin and angiostatin
23
Q
Why is angiogenesis important?
A
1) Necessary for tumor growth beyond about 1mm
2) A normal process in menstruation and pregnancy
3) An important adaptation of chronically exercised trained muscle
4) An adaptation to chronic ischemia
24
Q
How do arterioles branch within a tissue?
A
From larger to smaller
25
How many layers of SMC do arterioles have?
1-3
26
What is the average diameter for a arteriole?
< 100 µm
27
What size are the smallest arterioles that feed capillaries?
~10-15µm
28
What does a microvascular unit consist of?
1 arteriole, the capillaries it supplies, and the collecting venule(~15µm)
29
What are post capillary venules made of?
Only pericytes, no SMC
30
What size venules have SMCs?
>30-50µm
31
How permeable to water are post-capillary venules?
Very permeable
32
What is the capillary density of skeletal muscle?
300-1000 capillaries/mm^2 (1-3 capillaries/muscle fiber)
33
How can endurance exercise training change the capillary density in skeletal muscle?
increases to ~6-8 capillaries/muscle fiber
34
What is the capillary density of the heart and brain?
~3000 capillaries/mm^2
35
What does a greater capillary concentration in a tissue provide?
- Greater surface area for gas, water and solute exchange
| - Shorter diffusion distance
36
What is rhythmic contraction of arterioles called?
Vasomotion
37
What is the vasomotion cycling rate in muscle?
~15 cycles/min
38
What is transit time?
The time required for blood to flow through the capillary- so, the time allowed for gas and nutrient exchange
39
What is the transit time in resting muscle?
~0.5-2s
40
What is the transit time in exercising muscle?
~0.25s
41
Where are continuous capillaries found?
Skeletal muscle, skin, lung, fat, and nervous tissue
42
Describe the permeability of continuous capillaries.
Water, hydrophobic solutes, and small solutes can pass through tight junctions or by vesicular transport (Tight jx pores are ~4-5nm wide)
43
Where are fenestrated capillaries found?
Kidney, exocrine glands, intestinal mucosa, etc
44
Describe the permeability of fenestrated capillaries.
More permeable (~10-100X) than continuous capillaries
45
What are the fenestrae of fenestrated capillaries?
Sites of EC that are thin and perforated (~50-60nm wide)
46
Where are discontinuous capillaries found?
Bone marrow, live, and spleen
47
Describe the permeability of discontinuous capillaries.
Large gaps (>100mm) between ECs and discontinuous basal lamina
48
What do discontinuous capillaries allow into the blood?
Plasma proteins, RBCs, and WBCs
49
What dictates water flux?
Pressure gradients
50
What dictates solute flux?
Concentration gradient
51
What type of processes are water and solute flux?
Passive processes
52
What is flicks law of diffusion?
Js= -D A ∆C
53
What provides the surface area for lipophilic molecule diffusion?
The whole membrane
54
What provides the surface area for small hydrophilic molecule diffusion?
Can only diffuse through pores
55
What does the diffusion coefficient tell you?
- The ease of movement of a solute through a solvent
| - The hydrodynamic resistance, which depends on size and shape of molecule and viscosity of solvent
56
What is the stokes einstein equation?
D= kT/ 6πµnr
57
D is reduced to Dm because of?
1) Steric exclusion
| 2) Restricted diffusion
58
What is restricted diffusion?
Larger molecules compared to pore size (a/r) leaves less space for the solvent to flow around and carry the molecule
59
What effect does fluid have on larger molecules?
Hydrodynamic drag
60
What is Dm?
Effective diffusion coefficient
61
What is the formula for permeability?
P = D / ∆X= Js/ A ∆C
62
What 3 things does permeability depend on?
1) Ratio of radius to pore radius
2) Pore area relative to surface area (the extent of breaks in the tight junction)
3) Length of pore
63
What are the three types of molecules that move through these cells?
1) Lipid soluble (oxygen, steroids)
2) Small lipid insoluble (ions, glucose, amino acids, norepinephrine)
3) Large lipid insoluble molecules (Plasma proteins)
64
Describe the permeability of lipid soluble molecules.
- High permeability
| - Can pass through cell membrane
65
Where do small lipid-insoluble molecules diffuse through?
Water-filled intracellular junctions or fenestrations
66
What is the average pore size for small lipid-insoluble molecules?
4-5nm
67
How does permeability vary across continuous capillaries?
- Can be 10-fold difference between tissues
- Differences are due to differences in pore number, not pore size
- Permeability is proportional to the number of breaks in tight junction strands
68
What is glycocalyx made up of?
Negatively-charged, long, branched bipolymers (Glycoproteins, proteoglycans)
69
How does glycocalyx interact with albumin?
Binds albumin, which contributes to reduced permeability
70
What does glycocalyx repel?
Negatively charged molecules
71
What does the glycocalyx do to pore size?
Reduces effective pore size from 20nm to 4-5nm but covering the entrance to the cleft
72
What is the endothelial surface layer composed of?
Glycocalyx and attached plasma proteins and glycosaminoglycans
73
What does all the stuff attached to the endothelial surface layer do?
Decreases the area within the capillary available for blood flow
74
What does shear stress do in glycocalyx regulation?
Increased shear stress-> Increased thickness and charge of glycocalyx-> Decreased uptake of plasma proteins
75
What do ischemia and inflammation do in glycocalyx regulation?
Ischemia and inflammation-> changes in composition of proteoglycans-> Increased permeability
76
What does VEGF do in glycocalyx regulation?
May partially degrade glycocalyx
77
What does oxidized LDL do in glycocalyx regulation?
Ox-LDL-> Degrades glycocalyx-> Increased leukocyte adhesion
78
Where are large pores for large lipid-insoluble molecules present?
Continuous capillaries
79
How does the size of a large pore compare to the size of small pores?
~1 large pore: 4000 small pores
80
Where are no large pores found?
Cerebral and renal capillaries
81
What two things could large pores be?
1) Transendothelial channels
| 2) Caveolar-vesicular transport
82
What types of proteins cross endothelial cell membranes more readily?
- Smaller proteins
| - Positively charged proteins
83
What kind of pores does the blood brain barrier have?
- No intercellular pores
| - Very little caveolar-vesicular transport
84
How is transport carried out with the blood brain barrier?
- Nearly all carrier-mediated (except lipid-soluble molecules that can pass through the EC membrane)
- Specific carriers for specific molecules
85
How do most carriers facilitate diffusion?
Down its concentration gradient (does not require ATP), either into or out of the brain
86
What can cause a break down in the blood brain barrier?
- Acute hypertension
- Stroke
- Hemmorage
- Inflammation
87
What does a cerebral edema do?
Kill neurons
88
What happens to solute concentration within the capillary as the solute diffuses out?
It drops, so ∆C is always changing
89
Where is Js the greatest and why?
At the entrance to the capillary because ∆C is greatest here
90
What three things can determine solute exchange across an entire capillary bed?
- Arterial concentration of solute
- Venous concentration of solute
- Blood flow
91
What is the effect of blood flow on solute clearance for molecules with high permeability such as oxygen?
-> Flow limited (the higher the flow, the greater the solute flux
92
What is the effect of blood flow on solute clearance for molecules with moderate permeability such as glucose?
- > flow limited at low flows
| - > Diffusion-limited at high flows
93
What is the effect of blood flow on solute clearance for molecules with low permeability such as albumin?
-> diffusion limited (Diffusion is already maximal, increases in flow don't increase flux)
94
What effect does increased flow have on permeability?
Increases permeability through possible nitric oxide mediated ways
95
How can the surface area for solute flux be altered?
- >By opening (recruiting) more capillaries
| - > Increasing flow, if the molecule is flow limited
96
How can the concentration gradient (∆C) be altered?
Increased by either increase in blood concentration or decrease in tissue concentration of the solute
97
What is the path of water flow through compartments?
Intravascular->Interstitial->Lymphatics->vena cava-> Entire plasma volume circulated 1x/day
98
What 4 pressure dictate capillary water flux?
Pc-> Capillary blood pressure (hydraulic pressure)
Pi-> Interstitial hydraulic pressure
πp-> Plasma colloid osmotic (oncotic) pressure
πi-> interstitial colloid osmotic pressure
99
What is the formula for water flux?
(Pc-Pi)-(πp-πi) OR Filtering force - absorptive force
100
What is the starling equation for fluid exchange?
Jv = LpS [(Pc-Pi)-sigma(πp-πi)]
101
What is Lp?
Hydraulic conductance which is similar to permeability
102
What is S in the sterling equation?
Surface area
103
What is sigma in the sterling equation?
reflection coefficient for plasma proteins
104
What is the range for reflection coefficient for plasma proteins?
1 means no plasma proteins get through
| 0 means all plasma proteins get through
105
What is the usual number for the reflection coefficient for plasma proteins?
~0.8-0.95
106
What is filtration rate highly dependent on?
Capillary pressure (the most variable force in the starling equation)
107
What causes pressure to drop along the capillary?
Resistance to flow
108
What 4 things does capillary pressure depend on?
1) Length of capillary
2) Arterial and venous pressure
3) Resistance
4) Gravity
109
What happens to pressure as a capillary gets longer?
The longer the capillary the greater the pressure drop
110
When does capillary radius increase?
With flow and shear stress
111
What does flow do to the glycocalyx and the capillaries?
It may flatten the glycocalyx and increase the effective radius of the capillary
112
What cascade effects does increased venous pressure have on capillaries?
Increases capillary pressure-> Promotes capillary filtration-> Edema
113
How does pressure in arteries, veins, and capillaries change with distance below the heart?
Increases linearly with increase in distance below the heart when in an upright posture
114
What do arterioles do to counteract the pressure caused by gravity in the lower limbs?
Constrict to compensate and reduce capillary pressure
115
What does πp mean?
Plasma colloid osmotic pressure
116
What is πp about equal to?
Mid-capillary pressure
117
What primarily causes the pressure of πp?
Albumin
118
What does πi mean?
Interstitial colloid osmotic pressure
119
Is πi high or low in the leg?
low
120
Is πi high or low in the lung?
High
121
What is the concentration of protein in the interstitium dependent on?
Water flux
122
What effect does high water flux (Filtration) have on Ci?
Causes lower Ci
123
What effect does lower water flux (Absorption) have on Ci?
Greater Ci
124
Why is Js for protein relatively stable?
It is diffusion limited
125
What are the 4 main components of the interstitial matrix?
1) Collagen
2) Hyaluronan
3) Proteoglycans
4) Glycoproteins
126
What does collagen do in the interstitial matrix?
Provides structural support to the interstitial space
127
What do proteoglycans do in the interstitial matrix?
Contain branches of glycosaminoglycan chains (GAG's) which are negatively charged (Binds to sodium and attracts water) and provide resistance to flow
128
What effect does vasomotion have on filtration and absorption?
It causes periods of both, which can reduce overall filtration of water from capillaries over time
129
What causes the steep drop in pressure when interstitial volume goes below the normal level?
The GAGs in the interstitium cause a suctioning effect called "gel swelling pressure" which causes a low compliance
130
Why is water readily absorbed by the interstitium and hard to displace?
Because of the hydraulic conductivity of the interstitium due to the small pores that it contains formed by the connective tissue components
131
What is an edema?
Large pools of free water in the interstitial compartment that are not absorbed by intersitial proteins
132
What happens to water and solutes escaping from the capillaries?
They are picked up by the terminal lymphatic vessels, pumped into the thoracic duct, and returned to the venous system
133
What three main functions does the lymphatic system serve?
1) Preservation of fluid balance
2) Absorption of fat in the intestinal villi
3) Immune function
134
What is the immune function of lymph?
It clears foreign particles from the tissues and carries it to the lymph nodes where immune cells reside
135
What do lymph nodes contain?
Lymphocytes and their own blood supply
136
What happens once foreign materials enter a lymph node?
Activates lymphocytes which are carried into the circulation by the lymph
137
How do immune cells re-enter the lymph node?
Through gaps between the high endothelial cells in the nodal vein
138
What are the collecting vessels of the lymphatic system?
Lymphatic capillaries
139
What do lymphatic capillaries do?
Collect lymph (Interstitial fluid)
140
How big are lymphatic capillaries?
10-50um
141
What are lymphatic capillaries composed of?
Single layer of endothelial cells
142
What holds lymphatic vessels open?
Anchoring filaments
143
Why does interstitial usually flow into lymphatic vessels?
Because pressure in lymphatic vessels is low
144
What does tissue compression do to lymph?
Causes lymph from interstitium to move into lymphatic capillaries, and from lymphatic capillaries into collecting lymphatics
145
What causes lymphatic vessels to re-expand after compression?
Tension form anchoring filaments
146
What does rate of lymph flow into lymphatic capillaries depend on?
Interstitial volume and Pi
147
What 4 things promote flow of lymph?
1) Skeletal muscle pump
2) Respiratory muscle pump
3) Deformation of tissue with movement
4) Smooth muscle contraction in larger lymphatics
148
Why is smooth muscle contraction necessary to move lymph along larger lymphatic vessels?
Because venous pressure > Lymphatic pressure, so lymphatic pressure must be increased to empty lymph into veins
149
What prevents back flow in larger lymphatic vessels?
One-way valves
150
Describe the smooth muscle cell contractions in larger lymphatic vessels.
- > Spontaneous, rhythmic (8-15 cycles/min)
- > Initiated by pace maker cells that fire in each segment
- > These cells generate APs due to opening of fast Na channels and L-type Ca channels
- Contractions similar to cardiac cycle
151
What causes lymphatic stroke volume and contraction frequency to increase?
- Distension
| - Sympathetic stimulation (Important after hemorrhage)
152
How much protein is in lymph produced by the liver?
30-50%
153
How much protein is in lymph produced by the intestine?
~37%
154
How much protein is in lymph produced by the lung?
~6%
155
How much protein is in lymph produced by the kidney?
~8%
156
What does muscle contraction do with acute local edema?
Causes dilation of resistance vessels-> Increased Pc, increased Capillary recruitment-> increased surface area, lactate, and K+ release from muscle-> Increased πi
157
Increased Pc, Surface area, πi->
Increased Jv
158
What does hard exercise do to local edema?
Decreases plasma volume-> Compensatory water absorption from interstitium of non-exercising tissues
159
What is pathological edema?
Chronic excess interstitial fluid due to many causes
160
What is bad about pathological edema?
Detrimental because excess interstitial fluid increases diffusion distance from capillary cells
161
Where is pathological edema most dangerous?
In the lung
162
Why is pathological edema most dangerous in the lung?
- > Prevents normal inflation
- > edema can cross into alveoli and cause death
- > Often caused by left ventricular failure
163
Tissue swelling rate=?
Capillary filtration rate- lymphatic drainage rate
164
What happens when venous pressure is raised and what causes it?
Increased Pc, which causes edema
- > Right ventricular failure
- >Over transfusion
- > Deep vein thrombosis
- > Gravity (Ankles, sacrum)
165
What happens when the absorptive force into the capillary is decreased and what causes it?
Decreased πp, which causes edema
- >malnutrition (inadequate protein)
- > Intestinal malabsorption of protein
- > Kidney disease (protein leakage into urine)
- > Liver disease (Decreased synthesis of plasma protein)
166
What happens with lymphatic insufficiency and what causes it?
Edema
- > Idiopathic (poor development of lymphatics)
- > Damage (surgery)
- > Worm infestation - filariasis
167
What happens with inflammation and edemas and what causes it?
Edema
| -> Increased Lp, Decreased reflection coefficient, increased Pc
168
What inflammatory mediators cause transient increases in permeability?
Histamine, serotonin, bardykinin
169
What inflammatory mediators cause long-lasting increases in permeability?
VEGF, thrombin
170
What does chronic inflammation cause?
- Increased VEGF
- Activate leukocytes-> Release leukotrienes, PAF, superoxide, H2O2, elastase-> Causes damage to endothelium and chronic increased permeability
171
What can be used to treat chronic inflammation?
Steroids
172
How do steroids decrease chronic inflammation?
Inhibit leukocyte migration/activation, gap formation, vasodilation
173
What shape is smooth muscle?
Long and spindle shaped
174
What anchors the network of actin-myosin filaments in smooth muscle?
Dense bodies (cytoplasmic) and dense bands (membranes)
175
What difference is there between actin myosin filaments between smooth muscle and cardiac/skeletal muscle?
Filaments are much longer which allows for a large magnitude of shortening
176
What two things do smooth muscle actin-myosin filaments lack that other mucles actin-myosin filaments have?
No Z-lines
| Not striated because actin filaments are not parallel
177
Describe the SR in a smooth muscle cell.
Small, poorly developed calcium containing SR
178
What are the differences between potentials in cardiac/skeletal muscle and vascular smooth muscle?
Cardiac/skeletal has action potentials
-Vascular smooth has graded membrane potentials which contract proportionally to depolarization
179
What are the differences between contractile force regulation in cardiac/skeletal muscle and vascular smooth muscle?
Cardiac/skeletal contractile force is regulated by Ca concentration
-Vascilar smooth contractile force is regulated by both Ca concentration and sensitivity
180
What are the differences between regulation of actin-myosin x-bridge cycling in cardiac/skeletal muscle and vascular smooth muscle?
Cardiac/skeletal regulated by actin activation
-Vascular smooth regulated by myosin activation (however actin may be involved in Ca sensitivity)
181
What are the differences between contraction duration in cardiac/skeletal muscle and vascular smooth muscle?
Cardiac/skeletal has short duration contraction or twitch ~300ms
-Vascular smooth has sustained contraction w/low ATP usage (~1/300th of striated muscle)
182
Why does vascular smooth muscle contract for so long?
- Slow actin-myosin x-bridge cycling or no cycling, called "latch bridge"
- Contraction rate ~1/10 of striated muscle
183
What is the smooth muscle membrane potential in most vessels (particularly small arteries and arterioles)?
-50mV
184
What causes the baseline contraction (basal tone) in smooth muscle cells?
Small amount of calcium influx at rest
185
What does Kir do?
-Responsible for resting membrane potential
186
When is the Kir channel activated?
During exercise by increased K+ (extracellular)
| Hyperpolarization
187
What activates Katp?
Metabolic state
188
What does Kca do?
Modulates calcium influx and membrane potential
189
What does Kv do?
Stabilizes membrane potential
190
What blocks Kir?
Barium
191
What blocks Katp?
High ATP
| Glibenclamide
192
What blocks Kca?
TEA
| iberiotoxin
193
What blocks Kv (delayed rectifier)?
4-AP
194
What activates Katp?
Cromakalin
CGRP
Decreased intracellular ATP
Increased intracellular ADP
195
What activates Kca?
May be tonically active
Increased intracellular calcium
depolarization
196
What activates Kv?
Depolarization
197
What are the two voltage sensitive Ca channels?
L-type (long lasting)
| T-type (Transient, more important in arterioles)
198
What are some features of ROC's (receptor operated Ca channels)?
- Directly coupled to receptor
- Don't require depolarization for activation
- Some permeability to K and Na
199
What can activate non-selective cation channels?
- some by DAG
| - Some by stretch (TRP)
200
What type of channels may be responsible for depolarization during agonist-induced contraction?
Non-selective cation channels, chloride channels
201
What types of ions mainly pass through non-selective cation channels?
Ca and Na
202
What activates chloride channels?
Rise in calcium
203
What are chloride channels responsible for?
Basal membrane potential
204
Name some substances that can cause smooth muscle cell contraction.
- Norepi, ATP, nuropeptide Y
- Angiotensin II
- Endothelin
- Serotonin
- Thromboxane
- Vasopressin
205
What are some extracellular environment factors that can cause smooth muscle relaxation?
- Increased extracellular K-> Increased Kir activity-> Hyperpol-> Decreased L-type Ca activity
- Hypoxia-> Lowered ATP, Increased ADP-> Increased Katp channel activity-> Hyperpol-> Decreased L-type Ca activity
- Tissue metabolites
206
What are some neurotransmitters that can cause smooth muscle cell relaxation?
- CGRP, VIP
| - NE, E when beta 2 receptors are prominent
207
What type of nerves release CGRP, VIP?
Sensory nerves
208
What type of nerves release NE, E?
Sympathetic nerves
209
What are some endothelium derived substances that can cause smooth muscle cell relaxation?
NO, PGI2, EDHF
210
What are some inflammatory agents that can cause smooth muscle cell relaxation?
Histamine, VEGF, bradykinin, etc
211
What are the 3 major mechanisms for SMC relaxation?
1) Increased cAMP
2) Increased cGMP (e.g. NO)
3) Direct electrical coupling with endothelium (i.e. EDHF)
212
What physical forces control artery diameter?
Pressure
Flow
Temperature
213
What tissue factors control artery diameter?
Hypoxia
Metabolites
Inflammatory agents
214
What two things have systemic control of mean arterial pressure?
- Neural (ANS)
| - Hormonal (e.g. volume regulating hormones
215
What is basal tone?
Partial constriction of small arteries and arterioles under pressure
216
What causes basal tone?
1) Pressure (myogenic tone)
| 2) Release of factors from endothelium
217
What factors released from the endothelium take part in basal tone?
- Shear stress causes release of NO, PGI2 and EDHF, which decrease basal tone
- Some release of endothelin which increases basal tone
218
What is myogenic tone?
Contraction that originates in the smooth muscle and is due to stretch
219
What reaction does an artery have in myogenic tone to increases in pressure?
Expands briefly when pressure is raised, then constricts to a smaller than starting diameter
220
What is autoregulation?
As pressure increases, vessels constrict, which maintains flow through the tissue when there are acute changes in systemic pressure
221
What does autoregulation do for the brain?
Protects the brain tissue against fluctuations in arterial pressure
222
What does autoregulation do for the kidney?
Ensures constant glomerular filtration rate
223
What does autoregulation do that is not for the kidney and brain?
Keeps capillary pressure stable and prevents edema
224
What will inhibition of NOS do to basal tone?
Increase it, which means MAP goes up
225
What will blockade of ET receptors do to basal tone?
Slightly decrease it, which means MAP goes down
226
What are the two types of hyperemia?
1) Active hyperemia (also called functional or metabolic hyperemia
2) Reactive hyperemia (Increase in blood flow after occlusion)
227
When does active hyperemia happen?
With dynamic exercise
228
What is active hyperemia?
Blood flow increases rapidly, but there is an oxygen debt that must be repaid during recover
229
What factors in general account for active hyperemia?
Blood flow vs Oxygen demand
230
What is a main condition in tissue that partially accounts for exercise hyperemia?
Release of nitric oxide from red blood cells
231
Where is reactive hyperemia typically performed?
In the forearm
232
What happens to myogenic tone during reactive hyperemia?
It drops, which may partially account for the initial hyperemia
233
What are some mechanisms that may take part in reactive hyperemia?
1) Partly due to prostaglandins
| 2) Partly due to nitric oxide
234
What causes hyperpolarization of endothelial cells in arterioles within a tissue?
Hyperpolarizing charge moves between many endothelial cells through gap junctions
235
From greatest to smallest list the role of shear stress induced vasodilation on different sized arteries.
Conduit arteries
Small arteries
Large arterioles
Small arterioles
236
From greatest to smallest list the role of myogenic tone vasodilation on different sized arteries.
Small arterioles
Large arterioles
Small arteries
Conduit arteries
237
What does shear stress activate that can cause vasodilation?
eNOS
238
How do autonomic nerves control MAP?
Acutely
239
What are the 3 types of autonomic nerves that innervate blood vessels?
1) Sympathetic vasoconstrictor nerves (Most important and wide spread)
2) Sympathetic vasodilator nerves
3) Parasympathetic vasodilator nerves
240
What are the two sympathetic vasoconstrictor nerves?
```
VLM (Ventrolateral medulla- excitatory neurons)
Raphe nuclei (Inhibitory neurons)
```
241
What does nicotine from smoking cause nicotinic acetylcholine receptors in post-ganglionic cell bodies to do?
Increase Sympathetic Nerve Activity-> Vasoconstriction-> Increased Blood pressure
