Regulation of circulatory system Flashcards
(163 cards)
1
Q
What is vascular tone?
A
The state of partial constriction.
2
Q
What does the vascular tone establish?
A
A baseline of arteriolar resistance.
3
Q
Of what is the vascular tone a net effect?
A
Of Arteriolar Vasodilation.
Arteriolar vasoconstriction.
4
Q
What does the arteriolar vasodilation decrease?
A
Resistance.
5
Q
What does the arteriolar vasodilation increase?
A
Blood flow through the vessel.
6
Q
What does arteriole vasoconstriction increase?
A
Resistance.
7
Q
What does arterioles vasoconstriction decrease?
A
Flow.
8
Q
By what is arteriolar tone controlled?
A
By local/intrinsic controls and extrinsic controls.
9
Q
What is vasoconstriction?
A
Increased contraction of circular smooth muscle in the arteriolar wall.
10
Q
Where does vasoconstriction lead?
A
To increased resistance.
Decreased flow through the vessel.
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.
12
Q
What is vasodilation?
A
Decreased contraction of circular smooth muscle in the arteriolar wall.
13
Q
Where does vasodilation lead?
A
To decreased resistance.
Increased flow through the vessel.
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.
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.
16
Q
What does complementary action of precapillary sphincters and arterioles adjust?
A
Blood flow through a tissue.
17
Q
Why does complementary action of precapillary sphincter and arterioles adjust blood flow through a tissue?
A
In response to changing metabolic needs.
18
Q
In what is the extrinsic sympathetic control of arteriolar radius important?
A
In regulating blood pressure.
19
Q
What does increased sympathetic activity produce?
A
Generalized arteriolar vasoconstriction.
20
Q
Where does decreased sympathetic activity lead?
A
To generalized arteriolar vasodilation.
21
Q
What do the changes in arteriolar resistance bring?
A
Changes in mean arterial pressure.
22
Q
From where is NA released?
A
From sympathetic nerves.
23
Q
What does NA released from sympathetic nerves cause?
A
Vasoconstriction.
24
Q
What do skeletal and cardiac muscles have?
A
Local control mechanisms.
25
Why do skeletal and cardiac muscles have local control mechanisms?
To override sympathetic vasoconstriction during exercise.
26
Where is the cardiovascular control center?
In the medulla.
27
What does the cardiovascular control center in the medulla adjust?
Sympathetic output to the arterioles.
28
Which are the hormones that influence the blood pressure in the extrinsic control?
Adrenaline.
Noradrenaline.
Vasopressin.
Angiotensin 2.
29
What hormones are adrenaline and noradrenaline?
Adrenal medulla hormones.
30
What do adrenaline and noradrenaline hormones, influence?
Sympathetic tone.
31
In what are vasopressin and angiotensin 2 also important?
In controlling fluid balance.
32
What is the primary determinant of total peripheral resistance?
The adjustable arteriolar radius.
33
How many major categories of factors influence arteriolar radius?
2.
34
Which are the 2 major categories of factors that influence arteriolar radius?
1. Local/intrinsic control.
| 2. Extrinsic control.
35
In what is intrinsic control important?
In matching blood flow through a tissue with the tissue's metabolic needs.
36
By what is the intrinsic control mediated?
By local factors acting on the arteriolar smooth muscle.
37
In what is the extrinsic control important?
In regulating blood pressure.
38
By what is the extrinsic control mediated?
By sympathetic influence on arteriolar smooth muscle.
39
What do the venous valves prevent in their mechanical action?
Backflow of blood.
40
What is an example of a short term control measure?
The cardiac absorption effect from the empty atria.
41
What happens in the cardiac absorption effect from the empty atria?
The difference in pressure between the venae cavae and atria forces blood into fill the atria.
42
What does the action of the skeletal muscle pump increase?
Venous pressure.
43
What happens as we breathe in?
Our rib cage expands.
44
What does the rib cage increase, as it expands while we are breathing in?
The volume in our chest.
45
What does the expansion of our rib cage while we are breathing, decrease?
The pressure.
46
What effect does the decrease in pressure from expansion of our rib cage, while we are breathing, have?
The effect of increasing the pressure gradient between the chest and the rest of the body.
47
Why does the decreased pressure from our rib cage which expands while we are breathing, act?
To draw blood to the heart.
48
To what does the movement of interstitial fluid into the plasma contribute?
To the maintenance of the pressure.
49
What do longer term control measures include?
The actions of hormones.
50
What do hormones affect?
Kidney function.
| Fluid retention = hold.
51
Through what must the vascular tone be achieved in order to maintain BP?
Through the physiological balance of vasoconstriction and vasodilation of arterioles.
52
How is the physiological balance of vasoconstriction and vasodilation of arterioles (vascular tone) achieved to maintain BP?
Through intrinsic/local and extrinsic/neuronal control of smooth muscle tone.
53
How is the venous return characterised?
Passive.
54
By what is the venous return driven?
By action of heart, lungs and skeletal muscle.
55
What do endothelial cells form?
A single cell layer.
56
What does the single cell layer formed by the endothelial cells, line?
All blood vessels.
57
What does the single cell layer formed by the endothelial cells regulate?
Exchanges between the blood stream and the surrounding tissues.
58
What do the signals from endothelial cells organize?
The growth and development of connective tissue cells.
59
What do the connective tissue cells form?
The surrounding layers of the blood-vessel wall.
60
What do endothelial cells prevent?
Coagulation = freeze.
61
What do endothelial cells control?
Blood flow.
| Passage of proteins from blood into tissues.
62
What do endothelial cells inhibit?
Inflammation.
63
Where does the production of nitric oxide (NO) has a role?
In coagulation preventing.
Blood flow control.
Proteins passage from blood into tissues.
Inhibition of inflammation.
64
Of what is the insufficient NO production a major cause?
Of endothelial cell dysfunction.
65
Upon what does the basic mechanism involved in arteriole vasodilation rely?
Upon the production of NO.
66
How many enzymes utilise intracellular substrates to produce NO?
2.
67
Which are the 2 enzymes that utilise substrates to produce NO?
1. Endothelium NOS.
| 2. Cytochrome P450 reductase.
68
Across where does NO diffuse?
Across the lipid bilayers.
69
Why does NO diffuse across the lipid bilayers?
To cause relaxation of the smooth muscle.
70
To what is the endothelium extremely sensitive?
To Ach.
71
From what do the flow-mediated endothelial calcium responses arise?
From the autocrine action of non-neuronal ACh.
72
By what id the non-neuronal ACh released?
By the endothelium.
73
What does the increase in the rate of blood flow stimulate?
The endothelial cells to release Ach.
74
To what does Ach bind, once released form the endothelial cells?
To its receptor on the plasma membrane.
75
What does the Ach binding to its receptors on the plasma membrane initiate?
A signal transduction cascade.
76
What does the signal transduction cascade caused by Ach binding to its receptors initiation, cause?
The production of inositol triphosphate.
77
What does inositol triphosphate trigger?
Calcium release from the endoplasmic reticulum.
78
Where does the calcium released from the endoplasmic reticulum bind?
To the protein calmodulin.
79
What does the protein calmodulin activate?
NOS.
80
What does NOS produce?
NO.
81
Where does NO diffuse?
To the smooth muscle cells.
82
What does the NO activate once it diffuses to the smooth muscle cell?
The enzyme guanylate cyclase.
83
What does the enzyme guanylate cyclase convert?
GTP --> cGMP.
84
What does the elevated cGMP activate?
PKG.
85
What does PKG phosphorylate?
myosin light chain phosphatase.
86
What does the myosin light chain phosphatase dephosphorylate?
Myosin.
87
Why does the myosin light chain phosphatase dephosphorylate myosin?
To cause relaxation.
88
On what does relaxation depend?
On an intact endothelium.
89
What does addition of Ach cause?
An increase in diameter.
90
What does Ach become in case of Ach removal?
A vasoconstrictor.
91
Why does Ach become a vasoconstrictor hen Ach is removed?
Because it can act directly on the smooth muscle cell.
92
Why does Ach become a vasoconstrictor to act directly on the smooth muscle cell?
To increase intracellular calcium.
93
To who is the Ach becoming a vasoconstrictor to act directly on the smooth muscle cell to increase intracellular calcium a major issue?
For people with artery disease and damaged endothelium.
94
By what is BP determined?
By the combined activity of many systems.
95
Of what is the vasculature diameter a balance?
Of vasorelaxant and constrictor inputs across the entire body.
96
What does the brain have?
Direct sympathetic and parasympathetic innervations to the vasculature and heart.
97
Why does the brain have direct sympathetic and parasympathetic innervations to the vasculature and heart?
To influence vessel diameter and heart rate and force.
98
What else does the brain release?
Vasopressin.
99
What is vasopressin?
A peptide hormone.
100
On what does vasopressin act?
On the kidney.
101
Why does vasopressin act on the kidney?
To increase water absorption.
102
To what are the kidneys essential?
To BP regulation.
103
Why are the kidneys essential to BP regulation?
Due to the constant monitoring of BP.
| Production of aldosterone.
104
Of what is aldosterone part?
Of the very powerful vasoconstricting and retaining renin-aldosterone-angiotensin system.
105
By what is mean arterial pressure determined?
By cardiac output + total peripheral resistance.
106
By what is CO determined?
By heart rate + stroke volume.
107
By what are heart rate and stroke volume influenced?
By sympathetic activity.
| By adrenaline level.
108
What does parasympathetic activity decrease?
Heart rate.
109
By what is ventricular stroke volume increased?
By increased EDV.
110
By what is EDV increased?
By elevated atrial pressure.
111
By what is an increase in atrial pressure caused?
By increased venous return.
112
By what is an increased venous return caused?
By increased venous pressure.
| Increased blood volume.
113
What do angiotensin 2 and vasopressin increase?
Blood volume.
114
What does ANP decrease?
Blood volume.
115
By what is TPR determined?
By arteriole diameter.
116
By what is arteriole diameter determined?
By the balance of vasoconstrictor and vasodilator inputs.
117
What can vasoconstrictor and vasodilator inputs be in nature?
Extrinsic.
| Intrinsic.
118
By what else is TPR determined?
By blood viscosity.
119
With is the blood viscosity altered?
With the level of haematocrit or RBC's in the blood.
120
What do elevated RBCs increase?
Viscosity.
121
What system is the renin angiotensin aldosterone system?
A very powerful hormonal system.
122
What does the renin angiotensin aldosterone system provide?
Long term control of blood pressure.
123
For what is the renin angiotensin aldosterone system designed?
To respond when there is prolonged decrease in blood volume and/or osmolality.
124
What is osmolality?
The measure of solute concentration in the blood.
125
By what is Aof pressure sensed?
By baroreceptors in the carotid sinus.
126
By what else can the Aof pressure e activated?
By a decrease in the filtrate sodium chloride (NaCl) concentration.
By a decreased filtrate flow rate.
127
What does a decreased filtrate flow rate stimulate?
The macula densa in the nephron.
128
Why does the decreased filtrate flow rate stimulate the macula densa in the nephron?
To signal the adjacent juxtaglomerular cells --> release renin.
129
Where does renin act?
On the circulating peptide angiotensinogen.
130
By what is the circulating peptide angiotensinogen produced?
By the liver.
131
To what is the circulating peptide angiotensin converted?
To angiotensin 1.
132
To what is angiotensin 1 cleaved?
To angiotensin 2.
133
By what does angiotensin 1 cleave to angiotensin 2?
By ACE.
134
Where does ACE reside = κατοικεί?
On the apical/blood facing side of the epithelial cells in regions such as the lungs.
135
What are the actions of angiotensin 2 for?
To increase blood pressure.
136
What is an action of angiotensin 2 that increase blood pressure?
Action at the CNS.
137
Why does angiotensin 2 act at the CNS?
To increase sympathetic output.
| To stimulate the posterior pituitary.
138
Why would angiotensin 2 stimulate the posterior pituitary?
To release ADH.
139
Where does ADH act?
At the collecting duct of nephrons.
140
Why does ADH act at the collecting duct of nephrons?
To increase water absorption.
141
How else can angiotensin 2 be characterised?
As a powerful vasoconstrictor.
142
What can angiotensin 2 as a powerful vasoconstrictor?
Increase arteriole constriction.
143
What else does ANG2 stimulate?
Release of aldosterone from the adrenal cortex.
144
Where does aldosterone act?
At the collecting duct.
145
Why does aldosterone act at the collecting duct?
To increase sodium absorption.
146
Why do vasopressin and aldosterone act in communication?
To elevate blood volume.
147
How can vasopressin and aldosterone elevate blood volume?
By increasing water and salt absorption.
148
What is endothelin?
A powerful vasoconstrictor of VSM.
149
By which factors is the release of endothelin stimulated?
```
By ANG2.
ADH.
Cytokines.
Reactive oxygen specie.
Shearing forces.
--> acting on the vascular endothelium.
```
150
What does the release of endothelin cause?
The production of IP3.
| Increased intracellular calcium release.
151
What do the production of IP3 and the increased intracellular calcium release cause?
The activation of clamodulin and myosin light chai kinase enzyme.
152
What does myosin light chain kinase enzyme phosphorylate?
Myosin.
153
What does myosin facilitate?
Myosin interaction with actin filaments.
154
Why does myosin interact with actin filaments?
To produce contractile activity.
155
Where do vasoconstrictor actions of endothelin happen?
In the guinea pig coronary artery in the presence and absence of the endothelial lining.
156
In what does the removal of the endothelium result?
In a stronger constrictor response to 10nM endothelin.
157
What does the stronger constrictor response to 10nM endothelin from the removal of endothelium highlight?
The potent actions of endothelium.
| The effectiveness of the homeostatic actions of the endothelium.
158
What do the homeostatic actions of the endothelium release?
Basal levels of NO.
159
How are the affects of NO an endothelin on VSM tension and tone characterised?
Opposite effects.
160
What is the regulation of arterial BP?
A complex multi-system process.
161
What does the regulation of arterial BP process involve?
Acute and long-term regulators.
162
What is the RAAS system?
A hormone system.
163
What does the RAAS system regulate?
Blood pressure.
Fluid and electrolyte balance.
Systemic vascular resistance.
