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Cardiovascular physiology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What does damage to endothelium by high lipids, smoking, hypertension, etc provoke?

A

A immune response

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2
Q

What do immune cells become after they migrate under the endothelium?

A

Macrophages

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3
Q

What do macrophages in the endothelium due to damage do?

A

Take up lipid and cholesterol, especially oxidized-LDL

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4
Q

What is the next step in atherosclerosis after macrophage formation under the endothelium?

A

Smooth muscle cells migrate under endothelium and proliferate

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5
Q

What do SMCs and immune cells become under the endothelium?

A

Lipid-laden foam cells

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6
Q

What do lipid-laden foam cells form?

A

Fatty streak

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7
Q

What forms over a fatty streak over time that is susceptible to being ruptured under trauma?

A

Fibrous plaques

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8
Q

What happens to the fibrous plaques of atherosclerosis in advanced stages?

A

It becomes calcified with a core of dead cells

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9
Q

What stage of atherosclerosis is most likely to be the most life threatening?

A

The fibrous plaque stage

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10
Q

What is endothelial cell dysfunction mainly attributed to within the atherosclerotic process?

A

Decreased NO

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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

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12
Q

What type of effects does NO have?

A

Anti-atherogenic

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13
Q

What effect does superoxide have on NO?

A

It combines to form peroxynitrite, thereby reducing the bioavailability of NO

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14
Q

What does Peroxynitrite do?

A
  • Uncouples eNOS by oxidizing its cofactor BH4

- This causes eNOS to make superoxide

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15
Q

What effect does superoxide have on LDL?

A

It oxidizes LDL into its more atherogenic form

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16
Q

What type of blood vessels usually grow with angiogenesis?

A

Venules

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17
Q

What is arteriogenesis?

A

Growth and remodeling of pre-existing blood vessels

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18
Q

Where does arteriogenesis usually happen?

A

Arteries and arterioles

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19
Q

What is angiogenesis?

A

Growth of new blood vessels that sprout off of pre-existing vessels

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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

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21
Q

What happens to permeability in vessels as they age?

A

Hyper permeable when new, much less permeable as they develop

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22
Q

What antiangiogenic factors keep angiogenesis in check?

A

Thrombospondin and angiostatin

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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

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24
Q

How do arterioles branch within a tissue?

A

From larger to smaller

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25
Q

How many layers of SMC do arterioles have?

A

1-3

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26
Q

What is the average diameter for a arteriole?

A

< 100 µm

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27
Q

What size are the smallest arterioles that feed capillaries?

A

~10-15µm

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28
Q

What does a microvascular unit consist of?

A

1 arteriole, the capillaries it supplies, and the collecting venule(~15µm)

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29
Q

What are post capillary venules made of?

A

Only pericytes, no SMC

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30
Q

What size venules have SMCs?

A

> 30-50µm

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31
Q

How permeable to water are post-capillary venules?

A

Very permeable

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32
Q

What is the capillary density of skeletal muscle?

A

300-1000 capillaries/mm^2 (1-3 capillaries/muscle fiber)

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33
Q

How can endurance exercise training change the capillary density in skeletal muscle?

A

increases to ~6-8 capillaries/muscle fiber

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34
Q

What is the capillary density of the heart and brain?

A

~3000 capillaries/mm^2

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35
Q

What does a greater capillary concentration in a tissue provide?

A
  • Greater surface area for gas, water and solute exchange

- Shorter diffusion distance

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36
Q

What is rhythmic contraction of arterioles called?

A

Vasomotion

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37
Q

What is the vasomotion cycling rate in muscle?

A

~15 cycles/min

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38
Q

What is transit time?

A

The time required for blood to flow through the capillary- so, the time allowed for gas and nutrient exchange

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39
Q

What is the transit time in resting muscle?

A

~0.5-2s

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40
Q

What is the transit time in exercising muscle?

A

~0.25s

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41
Q

Where are continuous capillaries found?

A

Skeletal muscle, skin, lung, fat, and nervous tissue

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42
Q

Describe the permeability of continuous capillaries.

A

Water, hydrophobic solutes, and small solutes can pass through tight junctions or by vesicular transport (Tight jx pores are ~4-5nm wide)

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43
Q

Where are fenestrated capillaries found?

A

Kidney, exocrine glands, intestinal mucosa, etc

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44
Q

Describe the permeability of fenestrated capillaries.

A

More permeable (~10-100X) than continuous capillaries

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45
Q

What are the fenestrae of fenestrated capillaries?

A

Sites of EC that are thin and perforated (~50-60nm wide)

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46
Q

Where are discontinuous capillaries found?

A

Bone marrow, live, and spleen

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47
Q

Describe the permeability of discontinuous capillaries.

A

Large gaps (>100mm) between ECs and discontinuous basal lamina

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48
Q

What do discontinuous capillaries allow into the blood?

A

Plasma proteins, RBCs, and WBCs

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49
Q

What dictates water flux?

A

Pressure gradients

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50
Q

What dictates solute flux?

A

Concentration gradient

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51
Q

What type of processes are water and solute flux?

A

Passive processes

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52
Q

What is flicks law of diffusion?

A

Js= -D A ∆C

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53
Q

What provides the surface area for lipophilic molecule diffusion?

A

The whole membrane

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54
Q

What provides the surface area for small hydrophilic molecule diffusion?

A

Can only diffuse through pores

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55
Q

What does the diffusion coefficient tell you?

A
  • 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

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56
Q

What is the stokes einstein equation?

A

D= kT/ 6πµnr

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57
Q

D is reduced to Dm because of?

A

1) Steric exclusion

2) Restricted diffusion

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58
Q

What is restricted diffusion?

A

Larger molecules compared to pore size (a/r) leaves less space for the solvent to flow around and carry the molecule

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59
Q

What effect does fluid have on larger molecules?

A

Hydrodynamic drag

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60
Q

What is Dm?

A

Effective diffusion coefficient

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61
Q

What is the formula for permeability?

A

P = D / ∆X= Js/ A ∆C

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62
Q

What 3 things does permeability depend on?

A

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

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63
Q

What are the three types of molecules that move through these cells?

A

1) Lipid soluble (oxygen, steroids)
2) Small lipid insoluble (ions, glucose, amino acids, norepinephrine)
3) Large lipid insoluble molecules (Plasma proteins)

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64
Q

Describe the permeability of lipid soluble molecules.

A
  • High permeability

- Can pass through cell membrane

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65
Q

Where do small lipid-insoluble molecules diffuse through?

A

Water-filled intracellular junctions or fenestrations

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66
Q

What is the average pore size for small lipid-insoluble molecules?

A

4-5nm

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67
Q

How does permeability vary across continuous capillaries?

A
  • 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
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68
Q

What is glycocalyx made up of?

A

Negatively-charged, long, branched bipolymers (Glycoproteins, proteoglycans)

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69
Q

How does glycocalyx interact with albumin?

A

Binds albumin, which contributes to reduced permeability

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70
Q

What does glycocalyx repel?

A

Negatively charged molecules

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71
Q

What does the glycocalyx do to pore size?

A

Reduces effective pore size from 20nm to 4-5nm but covering the entrance to the cleft

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72
Q

What is the endothelial surface layer composed of?

A

Glycocalyx and attached plasma proteins and glycosaminoglycans

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73
Q

What does all the stuff attached to the endothelial surface layer do?

A

Decreases the area within the capillary available for blood flow

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74
Q

What does shear stress do in glycocalyx regulation?

A

Increased shear stress-> Increased thickness and charge of glycocalyx-> Decreased uptake of plasma proteins

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75
Q

What do ischemia and inflammation do in glycocalyx regulation?

A

Ischemia and inflammation-> changes in composition of proteoglycans-> Increased permeability

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76
Q

What does VEGF do in glycocalyx regulation?

A

May partially degrade glycocalyx

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77
Q

What does oxidized LDL do in glycocalyx regulation?

A

Ox-LDL-> Degrades glycocalyx-> Increased leukocyte adhesion

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78
Q

Where are large pores for large lipid-insoluble molecules present?

A

Continuous capillaries

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79
Q

How does the size of a large pore compare to the size of small pores?

A

~1 large pore: 4000 small pores

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80
Q

Where are no large pores found?

A

Cerebral and renal capillaries

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81
Q

What two things could large pores be?

A

1) Transendothelial channels

2) Caveolar-vesicular transport

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82
Q

What types of proteins cross endothelial cell membranes more readily?

A
  • Smaller proteins

- Positively charged proteins

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83
Q

What kind of pores does the blood brain barrier have?

A
  • No intercellular pores

- Very little caveolar-vesicular transport

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84
Q

How is transport carried out with the blood brain barrier?

A
  • Nearly all carrier-mediated (except lipid-soluble molecules that can pass through the EC membrane)
  • Specific carriers for specific molecules
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85
Q

How do most carriers facilitate diffusion?

A

Down its concentration gradient (does not require ATP), either into or out of the brain

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86
Q

What can cause a break down in the blood brain barrier?

A
  • Acute hypertension
  • Stroke
  • Hemmorage
  • Inflammation
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87
Q

What does a cerebral edema do?

A

Kill neurons

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88
Q

What happens to solute concentration within the capillary as the solute diffuses out?

A

It drops, so ∆C is always changing

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89
Q

Where is Js the greatest and why?

A

At the entrance to the capillary because ∆C is greatest here

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90
Q

What three things can determine solute exchange across an entire capillary bed?

A
  • Arterial concentration of solute
  • Venous concentration of solute
  • Blood flow
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91
Q

What is the effect of blood flow on solute clearance for molecules with high permeability such as oxygen?

A

-> Flow limited (the higher the flow, the greater the solute flux

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92
Q

What is the effect of blood flow on solute clearance for molecules with moderate permeability such as glucose?

A
  • > flow limited at low flows

- > Diffusion-limited at high flows

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93
Q

What is the effect of blood flow on solute clearance for molecules with low permeability such as albumin?

A

-> diffusion limited (Diffusion is already maximal, increases in flow don’t increase flux)

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94
Q

What effect does increased flow have on permeability?

A

Increases permeability through possible nitric oxide mediated ways

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95
Q

How can the surface area for solute flux be altered?

A
  • > By opening (recruiting) more capillaries

- > Increasing flow, if the molecule is flow limited

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96
Q

How can the concentration gradient (∆C) be altered?

A

Increased by either increase in blood concentration or decrease in tissue concentration of the solute

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97
Q

What is the path of water flow through compartments?

A

Intravascular->Interstitial->Lymphatics->vena cava-> Entire plasma volume circulated 1x/day

98
Q

What 4 pressure dictate capillary water flux?

A

Pc-> Capillary blood pressure (hydraulic pressure)
Pi-> Interstitial hydraulic pressure
πp-> Plasma colloid osmotic (oncotic) pressure
πi-> interstitial colloid osmotic pressure

99
Q

What is the formula for water flux?

A

(Pc-Pi)-(πp-πi) OR Filtering force - absorptive force

100
Q

What is the starling equation for fluid exchange?

A

Jv = LpS [(Pc-Pi)-sigma(πp-πi)]

101
Q

What is Lp?

A

Hydraulic conductance which is similar to permeability

102
Q

What is S in the sterling equation?

A

Surface area

103
Q

What is sigma in the sterling equation?

A

reflection coefficient for plasma proteins

104
Q

What is the range for reflection coefficient for plasma proteins?

A

1 means no plasma proteins get through

0 means all plasma proteins get through

105
Q

What is the usual number for the reflection coefficient for plasma proteins?

A

~0.8-0.95

106
Q

What is filtration rate highly dependent on?

A

Capillary pressure (the most variable force in the starling equation)

107
Q

What causes pressure to drop along the capillary?

A

Resistance to flow

108
Q

What 4 things does capillary pressure depend on?

A

1) Length of capillary
2) Arterial and venous pressure
3) Resistance
4) Gravity

109
Q

What happens to pressure as a capillary gets longer?

A

The longer the capillary the greater the pressure drop

110
Q

When does capillary radius increase?

A

With flow and shear stress

111
Q

What does flow do to the glycocalyx and the capillaries?

A

It may flatten the glycocalyx and increase the effective radius of the capillary

112
Q

What cascade effects does increased venous pressure have on capillaries?

A

Increases capillary pressure-> Promotes capillary filtration-> Edema

113
Q

How does pressure in arteries, veins, and capillaries change with distance below the heart?

A

Increases linearly with increase in distance below the heart when in an upright posture

114
Q

What do arterioles do to counteract the pressure caused by gravity in the lower limbs?

A

Constrict to compensate and reduce capillary pressure

115
Q

What does πp mean?

A

Plasma colloid osmotic pressure

116
Q

What is πp about equal to?

A

Mid-capillary pressure

117
Q

What primarily causes the pressure of πp?

A

Albumin

118
Q

What does πi mean?

A

Interstitial colloid osmotic pressure

119
Q

Is πi high or low in the leg?

A

low

120
Q

Is πi high or low in the lung?

A

High

121
Q

What is the concentration of protein in the interstitium dependent on?

A

Water flux

122
Q

What effect does high water flux (Filtration) have on Ci?

A

Causes lower Ci

123
Q

What effect does lower water flux (Absorption) have on Ci?

A

Greater Ci

124
Q

Why is Js for protein relatively stable?

A

It is diffusion limited

125
Q

What are the 4 main components of the interstitial matrix?

A

1) Collagen
2) Hyaluronan
3) Proteoglycans
4) Glycoproteins

126
Q

What does collagen do in the interstitial matrix?

A

Provides structural support to the interstitial space

127
Q

What do proteoglycans do in the interstitial matrix?

A

Contain branches of glycosaminoglycan chains (GAG’s) which are negatively charged (Binds to sodium and attracts water) and provide resistance to flow

128
Q

What effect does vasomotion have on filtration and absorption?

A

It causes periods of both, which can reduce overall filtration of water from capillaries over time

129
Q

What causes the steep drop in pressure when interstitial volume goes below the normal level?

A

The GAGs in the interstitium cause a suctioning effect called “gel swelling pressure” which causes a low compliance

130
Q

Why is water readily absorbed by the interstitium and hard to displace?

A

Because of the hydraulic conductivity of the interstitium due to the small pores that it contains formed by the connective tissue components

131
Q

What is an edema?

A

Large pools of free water in the interstitial compartment that are not absorbed by intersitial proteins

132
Q

What happens to water and solutes escaping from the capillaries?

A

They are picked up by the terminal lymphatic vessels, pumped into the thoracic duct, and returned to the venous system

133
Q

What three main functions does the lymphatic system serve?

A

1) Preservation of fluid balance
2) Absorption of fat in the intestinal villi
3) Immune function

134
Q

What is the immune function of lymph?

A

It clears foreign particles from the tissues and carries it to the lymph nodes where immune cells reside

135
Q

What do lymph nodes contain?

A

Lymphocytes and their own blood supply

136
Q

What happens once foreign materials enter a lymph node?

A

Activates lymphocytes which are carried into the circulation by the lymph

137
Q

How do immune cells re-enter the lymph node?

A

Through gaps between the high endothelial cells in the nodal vein

138
Q

What are the collecting vessels of the lymphatic system?

A

Lymphatic capillaries

139
Q

What do lymphatic capillaries do?

A

Collect lymph (Interstitial fluid)

140
Q

How big are lymphatic capillaries?

A

10-50um

141
Q

What are lymphatic capillaries composed of?

A

Single layer of endothelial cells

142
Q

What holds lymphatic vessels open?

A

Anchoring filaments

143
Q

Why does interstitial usually flow into lymphatic vessels?

A

Because pressure in lymphatic vessels is low

144
Q

What does tissue compression do to lymph?

A

Causes lymph from interstitium to move into lymphatic capillaries, and from lymphatic capillaries into collecting lymphatics

145
Q

What causes lymphatic vessels to re-expand after compression?

A

Tension form anchoring filaments

146
Q

What does rate of lymph flow into lymphatic capillaries depend on?

A

Interstitial volume and Pi

147
Q

What 4 things promote flow of lymph?

A

1) Skeletal muscle pump
2) Respiratory muscle pump
3) Deformation of tissue with movement
4) Smooth muscle contraction in larger lymphatics

148
Q

Why is smooth muscle contraction necessary to move lymph along larger lymphatic vessels?

A

Because venous pressure > Lymphatic pressure, so lymphatic pressure must be increased to empty lymph into veins

149
Q

What prevents back flow in larger lymphatic vessels?

A

One-way valves

150
Q

Describe the smooth muscle cell contractions in larger lymphatic vessels.

A
  • > 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
Q

What causes lymphatic stroke volume and contraction frequency to increase?

A
  • Distension

- Sympathetic stimulation (Important after hemorrhage)

152
Q

How much protein is in lymph produced by the liver?

A

30-50%

153
Q

How much protein is in lymph produced by the intestine?

A

~37%

154
Q

How much protein is in lymph produced by the lung?

A

~6%

155
Q

How much protein is in lymph produced by the kidney?

A

~8%

156
Q

What does muscle contraction do with acute local edema?

A

Causes dilation of resistance vessels-> Increased Pc, increased Capillary recruitment-> increased surface area, lactate, and K+ release from muscle-> Increased πi

157
Q

Increased Pc, Surface area, πi->

A

Increased Jv

158
Q

What does hard exercise do to local edema?

A

Decreases plasma volume-> Compensatory water absorption from interstitium of non-exercising tissues

159
Q

What is pathological edema?

A

Chronic excess interstitial fluid due to many causes

160
Q

What is bad about pathological edema?

A

Detrimental because excess interstitial fluid increases diffusion distance from capillary cells

161
Q

Where is pathological edema most dangerous?

A

In the lung

162
Q

Why is pathological edema most dangerous in the lung?

A
  • > Prevents normal inflation
  • > edema can cross into alveoli and cause death
  • > Often caused by left ventricular failure
163
Q

Tissue swelling rate=?

A

Capillary filtration rate- lymphatic drainage rate

164
Q

What happens when venous pressure is raised and what causes it?

A

Increased Pc, which causes edema

  • > Right ventricular failure
  • > Over transfusion
  • > Deep vein thrombosis
  • > Gravity (Ankles, sacrum)
165
Q

What happens when the absorptive force into the capillary is decreased and what causes it?

A

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
Q

What happens with lymphatic insufficiency and what causes it?

A

Edema

  • > Idiopathic (poor development of lymphatics)
  • > Damage (surgery)
  • > Worm infestation - filariasis
167
Q

What happens with inflammation and edemas and what causes it?

A

Edema

-> Increased Lp, Decreased reflection coefficient, increased Pc

168
Q

What inflammatory mediators cause transient increases in permeability?

A

Histamine, serotonin, bardykinin

169
Q

What inflammatory mediators cause long-lasting increases in permeability?

A

VEGF, thrombin

170
Q

What does chronic inflammation cause?

A
  • Increased VEGF
  • Activate leukocytes-> Release leukotrienes, PAF, superoxide, H2O2, elastase-> Causes damage to endothelium and chronic increased permeability
171
Q

What can be used to treat chronic inflammation?

A

Steroids

172
Q

How do steroids decrease chronic inflammation?

A

Inhibit leukocyte migration/activation, gap formation, vasodilation

173
Q

What shape is smooth muscle?

A

Long and spindle shaped

174
Q

What anchors the network of actin-myosin filaments in smooth muscle?

A

Dense bodies (cytoplasmic) and dense bands (membranes)

175
Q

What difference is there between actin myosin filaments between smooth muscle and cardiac/skeletal muscle?

A

Filaments are much longer which allows for a large magnitude of shortening

176
Q

What two things do smooth muscle actin-myosin filaments lack that other mucles actin-myosin filaments have?

A

No Z-lines

Not striated because actin filaments are not parallel

177
Q

Describe the SR in a smooth muscle cell.

A

Small, poorly developed calcium containing SR

178
Q

What are the differences between potentials in cardiac/skeletal muscle and vascular smooth muscle?

A

Cardiac/skeletal has action potentials

-Vascular smooth has graded membrane potentials which contract proportionally to depolarization

179
Q

What are the differences between contractile force regulation in cardiac/skeletal muscle and vascular smooth muscle?

A

Cardiac/skeletal contractile force is regulated by Ca concentration

-Vascilar smooth contractile force is regulated by both Ca concentration and sensitivity

180
Q

What are the differences between regulation of actin-myosin x-bridge cycling in cardiac/skeletal muscle and vascular smooth muscle?

A

Cardiac/skeletal regulated by actin activation

-Vascular smooth regulated by myosin activation (however actin may be involved in Ca sensitivity)

181
Q

What are the differences between contraction duration in cardiac/skeletal muscle and vascular smooth muscle?

A

Cardiac/skeletal has short duration contraction or twitch ~300ms

-Vascular smooth has sustained contraction w/low ATP usage (~1/300th of striated muscle)

182
Q

Why does vascular smooth muscle contract for so long?

A
  • Slow actin-myosin x-bridge cycling or no cycling, called “latch bridge”
  • Contraction rate ~1/10 of striated muscle
183
Q

What is the smooth muscle membrane potential in most vessels (particularly small arteries and arterioles)?

A

-50mV

184
Q

What causes the baseline contraction (basal tone) in smooth muscle cells?

A

Small amount of calcium influx at rest

185
Q

What does Kir do?

A

-Responsible for resting membrane potential

186
Q

When is the Kir channel activated?

A

During exercise by increased K+ (extracellular)

Hyperpolarization

187
Q

What activates Katp?

A

Metabolic state

188
Q

What does Kca do?

A

Modulates calcium influx and membrane potential

189
Q

What does Kv do?

A

Stabilizes membrane potential

190
Q

What blocks Kir?

A

Barium

191
Q

What blocks Katp?

A

High ATP

Glibenclamide

192
Q

What blocks Kca?

A

TEA

iberiotoxin

193
Q

What blocks Kv (delayed rectifier)?

A

4-AP

194
Q

What activates Katp?

A

Cromakalin
CGRP
Decreased intracellular ATP
Increased intracellular ADP

195
Q

What activates Kca?

A

May be tonically active
Increased intracellular calcium
depolarization

196
Q

What activates Kv?

A

Depolarization

197
Q

What are the two voltage sensitive Ca channels?

A

L-type (long lasting)

T-type (Transient, more important in arterioles)

198
Q

What are some features of ROC’s (receptor operated Ca channels)?

A
  • Directly coupled to receptor
  • Don’t require depolarization for activation
  • Some permeability to K and Na
199
Q

What can activate non-selective cation channels?

A
  • some by DAG

- Some by stretch (TRP)

200
Q

What type of channels may be responsible for depolarization during agonist-induced contraction?

A

Non-selective cation channels, chloride channels

201
Q

What types of ions mainly pass through non-selective cation channels?

A

Ca and Na

202
Q

What activates chloride channels?

A

Rise in calcium

203
Q

What are chloride channels responsible for?

A

Basal membrane potential

204
Q

Name some substances that can cause smooth muscle cell contraction.

A
  • Norepi, ATP, nuropeptide Y
  • Angiotensin II
  • Endothelin
  • Serotonin
  • Thromboxane
  • Vasopressin
205
Q

What are some extracellular environment factors that can cause smooth muscle relaxation?

A
  • 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
Q

What are some neurotransmitters that can cause smooth muscle cell relaxation?

A
  • CGRP, VIP

- NE, E when beta 2 receptors are prominent

207
Q

What type of nerves release CGRP, VIP?

A

Sensory nerves

208
Q

What type of nerves release NE, E?

A

Sympathetic nerves

209
Q

What are some endothelium derived substances that can cause smooth muscle cell relaxation?

A

NO, PGI2, EDHF

210
Q

What are some inflammatory agents that can cause smooth muscle cell relaxation?

A

Histamine, VEGF, bradykinin, etc

211
Q

What are the 3 major mechanisms for SMC relaxation?

A

1) Increased cAMP
2) Increased cGMP (e.g. NO)
3) Direct electrical coupling with endothelium (i.e. EDHF)

212
Q

What physical forces control artery diameter?

A

Pressure
Flow
Temperature

213
Q

What tissue factors control artery diameter?

A

Hypoxia
Metabolites
Inflammatory agents

214
Q

What two things have systemic control of mean arterial pressure?

A
  • Neural (ANS)

- Hormonal (e.g. volume regulating hormones

215
Q

What is basal tone?

A

Partial constriction of small arteries and arterioles under pressure

216
Q

What causes basal tone?

A

1) Pressure (myogenic tone)

2) Release of factors from endothelium

217
Q

What factors released from the endothelium take part in basal tone?

A
  • Shear stress causes release of NO, PGI2 and EDHF, which decrease basal tone
  • Some release of endothelin which increases basal tone
218
Q

What is myogenic tone?

A

Contraction that originates in the smooth muscle and is due to stretch

219
Q

What reaction does an artery have in myogenic tone to increases in pressure?

A

Expands briefly when pressure is raised, then constricts to a smaller than starting diameter

220
Q

What is autoregulation?

A

As pressure increases, vessels constrict, which maintains flow through the tissue when there are acute changes in systemic pressure

221
Q

What does autoregulation do for the brain?

A

Protects the brain tissue against fluctuations in arterial pressure

222
Q

What does autoregulation do for the kidney?

A

Ensures constant glomerular filtration rate

223
Q

What does autoregulation do that is not for the kidney and brain?

A

Keeps capillary pressure stable and prevents edema

224
Q

What will inhibition of NOS do to basal tone?

A

Increase it, which means MAP goes up

225
Q

What will blockade of ET receptors do to basal tone?

A

Slightly decrease it, which means MAP goes down

226
Q

What are the two types of hyperemia?

A

1) Active hyperemia (also called functional or metabolic hyperemia
2) Reactive hyperemia (Increase in blood flow after occlusion)

227
Q

When does active hyperemia happen?

A

With dynamic exercise

228
Q

What is active hyperemia?

A

Blood flow increases rapidly, but there is an oxygen debt that must be repaid during recover

229
Q

What factors in general account for active hyperemia?

A

Blood flow vs Oxygen demand

230
Q

What is a main condition in tissue that partially accounts for exercise hyperemia?

A

Release of nitric oxide from red blood cells

231
Q

Where is reactive hyperemia typically performed?

A

In the forearm

232
Q

What happens to myogenic tone during reactive hyperemia?

A

It drops, which may partially account for the initial hyperemia

233
Q

What are some mechanisms that may take part in reactive hyperemia?

A

1) Partly due to prostaglandins

2) Partly due to nitric oxide

234
Q

What causes hyperpolarization of endothelial cells in arterioles within a tissue?

A

Hyperpolarizing charge moves between many endothelial cells through gap junctions

235
Q

From greatest to smallest list the role of shear stress induced vasodilation on different sized arteries.

A

Conduit arteries
Small arteries
Large arterioles
Small arterioles

236
Q

From greatest to smallest list the role of myogenic tone vasodilation on different sized arteries.

A

Small arterioles
Large arterioles
Small arteries
Conduit arteries

237
Q

What does shear stress activate that can cause vasodilation?

A

eNOS

238
Q

How do autonomic nerves control MAP?

A

Acutely

239
Q

What are the 3 types of autonomic nerves that innervate blood vessels?

A

1) Sympathetic vasoconstrictor nerves (Most important and wide spread)
2) Sympathetic vasodilator nerves
3) Parasympathetic vasodilator nerves

240
Q

What are the two sympathetic vasoconstrictor nerves?

A 
VLM (Ventrolateral medulla- excitatory neurons)
Raphe nuclei (Inhibitory neurons)
241
Q

What does nicotine from smoking cause nicotinic acetylcholine receptors in post-ganglionic cell bodies to do?

A

Increase Sympathetic Nerve Activity-> Vasoconstriction-> Increased Blood pressure

Cardiovascular physiology (3 decks)

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