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Regulation of circulatory system Flashcards

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USMLE® Step 1 flashcards
1
Q

What is vascular tone?

A

The state of partial constriction.

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2
Q

What does the vascular tone establish?

A

A baseline of arteriolar resistance.

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3
Q

Of what is the vascular tone a net effect?

A

Of Arteriolar Vasodilation.

Arteriolar vasoconstriction.

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4
Q

What does the arteriolar vasodilation decrease?

A

Resistance.

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5
Q

What does the arteriolar vasodilation increase?

A

Blood flow through the vessel.

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6
Q

What does arteriole vasoconstriction increase?

A

Resistance.

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7
Q

What does arterioles vasoconstriction decrease?

A

Flow.

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8
Q

By what is arteriolar tone controlled?

A

By local/intrinsic controls and extrinsic controls.

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9
Q

What is vasoconstriction?

A

Increased contraction of circular smooth muscle in the arteriolar wall.

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10
Q

Where does vasoconstriction lead?

A

To increased resistance.

Decreased flow through the vessel.

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11
Q

Which factors cause vasoconstriction?

A 
High myogenic activity.
High oxygen.
Low carbon dioxide.
Low other metabolites.
High endothelium.
High sympathetic stimulation.
Angiotensin 2.
Cold.
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12
Q

What is vasodilation?

A

Decreased contraction of circular smooth muscle in the arteriolar wall.

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13
Q

Where does vasodilation lead?

A

To decreased resistance.

Increased flow through the vessel.

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14
Q

Which factors cause vasodilation?

A 
Low myogenic activity.
Low oxygen.
High carbon dioxide.
High other metabolites. 
High nitric oxide.
Low sympathetic stimulation.
Histamine release.
Heat.
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15
Q

What are the local influences associated with increased metabolic activity/intrinsic control?

A 
Decreased oxygen.
Increased carbon dioxide.
Increased acid.
Increased K+.
Increased osmolality.
Adenosine release.
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16
Q

What does complementary action of precapillary sphincters and arterioles adjust?

A

Blood flow through a tissue.

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17
Q

Why does complementary action of precapillary sphincter and arterioles adjust blood flow through a tissue?

A

In response to changing metabolic needs.

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18
Q

In what is the extrinsic sympathetic control of arteriolar radius important?

A

In regulating blood pressure.

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19
Q

What does increased sympathetic activity produce?

A

Generalized arteriolar vasoconstriction.

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20
Q

Where does decreased sympathetic activity lead?

A

To generalized arteriolar vasodilation.

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21
Q

What do the changes in arteriolar resistance bring?

A

Changes in mean arterial pressure.

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22
Q

From where is NA released?

A

From sympathetic nerves.

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23
Q

What does NA released from sympathetic nerves cause?

A

Vasoconstriction.

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24
Q

What do skeletal and cardiac muscles have?

A

Local control mechanisms.

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25
Q

Why do skeletal and cardiac muscles have local control mechanisms?

A

To override sympathetic vasoconstriction during exercise.

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26
Q

Where is the cardiovascular control center?

A

In the medulla.

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27
Q

What does the cardiovascular control center in the medulla adjust?

A

Sympathetic output to the arterioles.

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28
Q

Which are the hormones that influence the blood pressure in the extrinsic control?

A

Adrenaline.
Noradrenaline.
Vasopressin.
Angiotensin 2.

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29
Q

What hormones are adrenaline and noradrenaline?

A

Adrenal medulla hormones.

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30
Q

What do adrenaline and noradrenaline hormones, influence?

A

Sympathetic tone.

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31
Q

In what are vasopressin and angiotensin 2 also important?

A

In controlling fluid balance.

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32
Q

What is the primary determinant of total peripheral resistance?

A

The adjustable arteriolar radius.

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33
Q

How many major categories of factors influence arteriolar radius?

A

2.

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34
Q

Which are the 2 major categories of factors that influence arteriolar radius?

A
  1. Local/intrinsic control.

2. Extrinsic control.

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35
Q

In what is intrinsic control important?

A

In matching blood flow through a tissue with the tissue’s metabolic needs.

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36
Q

By what is the intrinsic control mediated?

A

By local factors acting on the arteriolar smooth muscle.

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37
Q

In what is the extrinsic control important?

A

In regulating blood pressure.

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38
Q

By what is the extrinsic control mediated?

A

By sympathetic influence on arteriolar smooth muscle.

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39
Q

What do the venous valves prevent in their mechanical action?

A

Backflow of blood.

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40
Q

What is an example of a short term control measure?

A

The cardiac absorption effect from the empty atria.

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41
Q

What happens in the cardiac absorption effect from the empty atria?

A

The difference in pressure between the venae cavae and atria forces blood into fill the atria.

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42
Q

What does the action of the skeletal muscle pump increase?

A

Venous pressure.

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43
Q

What happens as we breathe in?

A

Our rib cage expands.

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44
Q

What does the rib cage increase, as it expands while we are breathing in?

A

The volume in our chest.

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45
Q

What does the expansion of our rib cage while we are breathing, decrease?

A

The pressure.

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46
Q

What effect does the decrease in pressure from expansion of our rib cage, while we are breathing, have?

A

The effect of increasing the pressure gradient between the chest and the rest of the body.

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47
Q

Why does the decreased pressure from our rib cage which expands while we are breathing, act?

A

To draw blood to the heart.

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48
Q

To what does the movement of interstitial fluid into the plasma contribute?

A

To the maintenance of the pressure.

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49
Q

What do longer term control measures include?

A

The actions of hormones.

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50
Q

What do hormones affect?

A

Kidney function.

Fluid retention = hold.

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51
Q

Through what must the vascular tone be achieved in order to maintain BP?

A

Through the physiological balance of vasoconstriction and vasodilation of arterioles.

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52
Q

How is the physiological balance of vasoconstriction and vasodilation of arterioles (vascular tone) achieved to maintain BP?

A

Through intrinsic/local and extrinsic/neuronal control of smooth muscle tone.

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53
Q

How is the venous return characterised?

A

Passive.

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54
Q

By what is the venous return driven?

A

By action of heart, lungs and skeletal muscle.

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55
Q

What do endothelial cells form?

A

A single cell layer.

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56
Q

What does the single cell layer formed by the endothelial cells, line?

A

All blood vessels.

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57
Q

What does the single cell layer formed by the endothelial cells regulate?

A

Exchanges between the blood stream and the surrounding tissues.

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58
Q

What do the signals from endothelial cells organize?

A

The growth and development of connective tissue cells.

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59
Q

What do the connective tissue cells form?

A

The surrounding layers of the blood-vessel wall.

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60
Q

What do endothelial cells prevent?

A

Coagulation = freeze.

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61
Q

What do endothelial cells control?

A

Blood flow.

Passage of proteins from blood into tissues.

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62
Q

What do endothelial cells inhibit?

A

Inflammation.

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63
Q

Where does the production of nitric oxide (NO) has a role?

A

In coagulation preventing.
Blood flow control.
Proteins passage from blood into tissues.
Inhibition of inflammation.

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64
Q

Of what is the insufficient NO production a major cause?

A

Of endothelial cell dysfunction.

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65
Q

Upon what does the basic mechanism involved in arteriole vasodilation rely?

A

Upon the production of NO.

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66
Q

How many enzymes utilise intracellular substrates to produce NO?

A

2.

67
Q

Which are the 2 enzymes that utilise substrates to produce NO?

A
  1. Endothelium NOS.

2. Cytochrome P450 reductase.

68
Q

Across where does NO diffuse?

A

Across the lipid bilayers.

69
Q

Why does NO diffuse across the lipid bilayers?

A

To cause relaxation of the smooth muscle.

70
Q

To what is the endothelium extremely sensitive?

A

To Ach.

71
Q

From what do the flow-mediated endothelial calcium responses arise?

A

From the autocrine action of non-neuronal ACh.

72
Q

By what id the non-neuronal ACh released?

A

By the endothelium.

73
Q

What does the increase in the rate of blood flow stimulate?

A

The endothelial cells to release Ach.

74
Q

To what does Ach bind, once released form the endothelial cells?

A

To its receptor on the plasma membrane.

75
Q

What does the Ach binding to its receptors on the plasma membrane initiate?

A

A signal transduction cascade.

76
Q

What does the signal transduction cascade caused by Ach binding to its receptors initiation, cause?

A

The production of inositol triphosphate.

77
Q

What does inositol triphosphate trigger?

A

Calcium release from the endoplasmic reticulum.

78
Q

Where does the calcium released from the endoplasmic reticulum bind?

A

To the protein calmodulin.

79
Q

What does the protein calmodulin activate?

A

NOS.

80
Q

What does NOS produce?

A

NO.

81
Q

Where does NO diffuse?

A

To the smooth muscle cells.

82
Q

What does the NO activate once it diffuses to the smooth muscle cell?

A

The enzyme guanylate cyclase.

83
Q

What does the enzyme guanylate cyclase convert?

A

GTP –> cGMP.

84
Q

What does the elevated cGMP activate?

A

PKG.

85
Q

What does PKG phosphorylate?

A

myosin light chain phosphatase.

86
Q

What does the myosin light chain phosphatase dephosphorylate?

A

Myosin.

87
Q

Why does the myosin light chain phosphatase dephosphorylate myosin?

A

To cause relaxation.

88
Q

On what does relaxation depend?

A

On an intact endothelium.

89
Q

What does addition of Ach cause?

A

An increase in diameter.

90
Q

What does Ach become in case of Ach removal?

A

A vasoconstrictor.

91
Q

Why does Ach become a vasoconstrictor hen Ach is removed?

A

Because it can act directly on the smooth muscle cell.

92
Q

Why does Ach become a vasoconstrictor to act directly on the smooth muscle cell?

A

To increase intracellular calcium.

93
Q

To who is the Ach becoming a vasoconstrictor to act directly on the smooth muscle cell to increase intracellular calcium a major issue?

A

For people with artery disease and damaged endothelium.

94
Q

By what is BP determined?

A

By the combined activity of many systems.

95
Q

Of what is the vasculature diameter a balance?

A

Of vasorelaxant and constrictor inputs across the entire body.

96
Q

What does the brain have?

A

Direct sympathetic and parasympathetic innervations to the vasculature and heart.

97
Q

Why does the brain have direct sympathetic and parasympathetic innervations to the vasculature and heart?

A

To influence vessel diameter and heart rate and force.

98
Q

What else does the brain release?

A

Vasopressin.

99
Q

What is vasopressin?

A

A peptide hormone.

100
Q

On what does vasopressin act?

A

On the kidney.

101
Q

Why does vasopressin act on the kidney?

A

To increase water absorption.

102
Q

To what are the kidneys essential?

A

To BP regulation.

103
Q

Why are the kidneys essential to BP regulation?

A

Due to the constant monitoring of BP.

Production of aldosterone.

104
Q

Of what is aldosterone part?

A

Of the very powerful vasoconstricting and retaining renin-aldosterone-angiotensin system.

105
Q

By what is mean arterial pressure determined?

A

By cardiac output + total peripheral resistance.

106
Q

By what is CO determined?

A

By heart rate + stroke volume.

107
Q

By what are heart rate and stroke volume influenced?

A

By sympathetic activity.

By adrenaline level.

108
Q

What does parasympathetic activity decrease?

A

Heart rate.

109
Q

By what is ventricular stroke volume increased?

A

By increased EDV.

110
Q

By what is EDV increased?

A

By elevated atrial pressure.

111
Q

By what is an increase in atrial pressure caused?

A

By increased venous return.

112
Q

By what is an increased venous return caused?

A

By increased venous pressure.

Increased blood volume.

113
Q

What do angiotensin 2 and vasopressin increase?

A

Blood volume.

114
Q

What does ANP decrease?

A

Blood volume.

115
Q

By what is TPR determined?

A

By arteriole diameter.

116
Q

By what is arteriole diameter determined?

A

By the balance of vasoconstrictor and vasodilator inputs.

117
Q

What can vasoconstrictor and vasodilator inputs be in nature?

A

Extrinsic.

Intrinsic.

118
Q

By what else is TPR determined?

A

By blood viscosity.

119
Q

With is the blood viscosity altered?

A

With the level of haematocrit or RBC’s in the blood.

120
Q

What do elevated RBCs increase?

A

Viscosity.

121
Q

What system is the renin angiotensin aldosterone system?

A

A very powerful hormonal system.

122
Q

What does the renin angiotensin aldosterone system provide?

A

Long term control of blood pressure.

123
Q

For what is the renin angiotensin aldosterone system designed?

A

To respond when there is prolonged decrease in blood volume and/or osmolality.

124
Q

What is osmolality?

A

The measure of solute concentration in the blood.

125
Q

By what is Aof pressure sensed?

A

By baroreceptors in the carotid sinus.

126
Q

By what else can the Aof pressure e activated?

A

By a decrease in the filtrate sodium chloride (NaCl) concentration.
By a decreased filtrate flow rate.

127
Q

What does a decreased filtrate flow rate stimulate?

A

The macula densa in the nephron.

128
Q

Why does the decreased filtrate flow rate stimulate the macula densa in the nephron?

A

To signal the adjacent juxtaglomerular cells –> release renin.

129
Q

Where does renin act?

A

On the circulating peptide angiotensinogen.

130
Q

By what is the circulating peptide angiotensinogen produced?

A

By the liver.

131
Q

To what is the circulating peptide angiotensin converted?

A

To angiotensin 1.

132
Q

To what is angiotensin 1 cleaved?

A

To angiotensin 2.

133
Q

By what does angiotensin 1 cleave to angiotensin 2?

A

By ACE.

134
Q

Where does ACE reside = κατοικεί?

A

On the apical/blood facing side of the epithelial cells in regions such as the lungs.

135
Q

What are the actions of angiotensin 2 for?

A

To increase blood pressure.

136
Q

What is an action of angiotensin 2 that increase blood pressure?

A

Action at the CNS.

137
Q

Why does angiotensin 2 act at the CNS?

A

To increase sympathetic output.

To stimulate the posterior pituitary.

138
Q

Why would angiotensin 2 stimulate the posterior pituitary?

A

To release ADH.

139
Q

Where does ADH act?

A

At the collecting duct of nephrons.

140
Q

Why does ADH act at the collecting duct of nephrons?

A

To increase water absorption.

141
Q

How else can angiotensin 2 be characterised?

A

As a powerful vasoconstrictor.

142
Q

What can angiotensin 2 as a powerful vasoconstrictor?

A

Increase arteriole constriction.

143
Q

What else does ANG2 stimulate?

A

Release of aldosterone from the adrenal cortex.

144
Q

Where does aldosterone act?

A

At the collecting duct.

145
Q

Why does aldosterone act at the collecting duct?

A

To increase sodium absorption.

146
Q

Why do vasopressin and aldosterone act in communication?

A

To elevate blood volume.

147
Q

How can vasopressin and aldosterone elevate blood volume?

A

By increasing water and salt absorption.

148
Q

What is endothelin?

A

A powerful vasoconstrictor of VSM.

149
Q

By which factors is the release of endothelin stimulated?

A 
By ANG2.
ADH.
Cytokines.
Reactive oxygen specie.
Shearing forces. 
--> acting on the vascular endothelium.
150
Q

What does the release of endothelin cause?

A

The production of IP3.

Increased intracellular calcium release.

151
Q

What do the production of IP3 and the increased intracellular calcium release cause?

A

The activation of clamodulin and myosin light chai kinase enzyme.

152
Q

What does myosin light chain kinase enzyme phosphorylate?

A

Myosin.

153
Q

What does myosin facilitate?

A

Myosin interaction with actin filaments.

154
Q

Why does myosin interact with actin filaments?

A

To produce contractile activity.

155
Q

Where do vasoconstrictor actions of endothelin happen?

A

In the guinea pig coronary artery in the presence and absence of the endothelial lining.

156
Q

In what does the removal of the endothelium result?

A

In a stronger constrictor response to 10nM endothelin.

157
Q

What does the stronger constrictor response to 10nM endothelin from the removal of endothelium highlight?

A

The potent actions of endothelium.

The effectiveness of the homeostatic actions of the endothelium.

158
Q

What do the homeostatic actions of the endothelium release?

A

Basal levels of NO.

159
Q

How are the affects of NO an endothelin on VSM tension and tone characterised?

A

Opposite effects.

160
Q

What is the regulation of arterial BP?

A

A complex multi-system process.

161
Q

What does the regulation of arterial BP process involve?

A

Acute and long-term regulators.

162
Q

What is the RAAS system?

A

A hormone system.

163
Q

What does the RAAS system regulate?

A

Blood pressure.
Fluid and electrolyte balance.
Systemic vascular resistance.

Medical Physiology (12 decks)

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