Control of blood flow Flashcards
1
Q
What are the two primary systems involved in the control of blood flow in different organs?
A
Sympathetic (neuronal) and Endocrine (hormonal) systems.
2
Q
What are autocoids in the context of blood flow control?
A
Local hormones that influence blood flow.
3
Q
What does “active hyperaemia” refer to in local blood flow control?
A
The increase in blood flow to tissues based on their metabolic activity.
4
Q
What is “flow autoregulation” in blood flow mechanisms?
A
The ability of tissues to maintain a consistent blood flow despite changes in perfusion pressure, involving local myogenic and metabolic factors.
5
Q
What role does the sympathetic nervous system play in blood vessel control?
A
The sympathetic nervous system, using noradrenaline, regulates blood vessel constriction and dilation via central control.
6
Q
Which part of the nervous system is responsible for central control of blood vessel tone?
A
The sympathetic nervous system.
7
Q
What is the role of sympathetic nerves in the vasculature?
A
Sympathetic nerves cause vasoconstriction, especially in the spleen, kidneys, skin, and muscles, by releasing noradrenaline that acts on α₁ receptors.
8
Q
Why is the sympathetic nervous system important for blood flow?
A
It redistributes blood flow and increases total peripheral resistance (TPR) to raise mean arterial pressure (MAP).
9
Q
What neurotransmitter and receptor are associated with parasympathetic nerves in vasodilation?
A
Acetylcholine acting on muscarinic receptors.
10
Q
Which organs are primarily affected by parasympathetic-induced vasodilation?
A
Salivary glands, pancreas, intestinal mucosa, and penis.
11
Q
Does parasympathetic nervous system (PNS) activation affect total peripheral resistance (TPR)?
A
No, PNS activation has no significant effect on TPR as it affects only a few vascular beds.
12
Q
In the provided image, what do the red and green structures represent?
A
Red represents smooth muscle cells, and green represents sympathetic nerve fibers.
13
Q
What two types of hormonal control regulate blood vessels?
A
Hormones in the blood and autocoids (local hormones).
14
Q
What are autocoids, and what role do they play in vascular control?
A
Autocoids are local hormones that mediate both direct and indirect dilation or constriction of blood vessels.
15
Q
What layer of the blood vessel is targeted by hormones to regulate vessel tone?
A
Hormones primarily act on the smooth muscle layer to regulate vasoconstriction or vasodilation.
16
Q
What is the role of the renin-angiotensin system in blood vessel control?
A
The kidneys release renin, which converts angiotensinogen into angiotensin II, causing vasoconstriction and raising total peripheral resistance (TPR) in response to reduced blood volume.
17
Q
How does anti-diuretic hormone (vasopressin) affect blood vessels?
A
Released by the posterior pituitary in response to dehydration, it causes vasoconstriction to help maintain blood pressure.
18
Q
What is the effect of adrenaline on blood vessels?
A
Adrenaline, released from the adrenal glands via SNS activation, can cause vasoconstriction or vasodilation depending on the receptors it acts upon.
19
Q
How does atrial natriuretic peptide (ANP) influence blood vessel tone?
A
ANP is released by the atria in response to increased blood volume and promotes vasodilation, lowering TPR.
20
Q
What are the two opposing effects of vasoactive hormones on TPR?
A
Angiotensin II: Raises TPR in response to low blood volume.]
ANP: Lowers TPR in response to high blood volume.
21
Q
Which neurotransmitter is more important at rest in mediating SNS effects on the cardiovascular system?
A
Noradrenaline
22
Q
Where is adrenaline secreted from, and under what conditions does its secretion increase?
A
Adrenaline is secreted by the adrenal medulla, with increased secretion during stressful situations such as fight or flight, hypotension, and hypoglycaemia.
23
Q
What receptor does noradrenaline primarily act on to cause vasoconstriction?
A
α₁ receptors, which mediate vasoconstriction via IP₃/DAG signaling.
24
Q
What receptor does adrenaline act on to increase heart rate and cardiac contractility?
A
β₁ receptors, which act via cAMP signaling.
25
What is the effect of adrenaline acting on β₂ receptors?
It causes vasodilation in skeletal muscles and the heart via cAMP signaling.
26
How much do adrenaline blood levels increase during stress?
Blood levels of adrenaline rise fivefold during stress.
27
Which local hormones are released by resident or infiltrating immune cells to cause vasodilation?
Histamine and Bradykinin.
28
What role does nitric oxide play in blood vessel regulation?
Nitric oxide, produced by the endothelium, mediates vasodilation.
29
Which local hormone is released by cardiac muscle to induce vasodilation?
Adenosine
30
What is the effect of thromboxane on blood vessels, and what cells release it?
Thromboxane, released by activated platelets, causes vasoconstriction.
31
What is the primary factor in metabolic control of blood flow?
Tissue metabolites, which are produced locally during metabolic activity.
32
How do tissue metabolites affect blood vessels?
Tissue metabolites cause direct vasodilation to increase blood flow to meet metabolic demands.
33
Which layer of blood vessels responds to tissue metabolites for metabolic control?
The endothelium and smooth muscle layers respond to tissue metabolites for vasodilation.
34
What is active hyperaemia?
It is the increase in blood flow to skeletal and cardiac muscles to match the increased metabolic demand during activity.
35
What sequence of events happen during exercise?
36
Which two muscle types are primarily involved in active hyperaemia?
Skeletal and cardiac muscles.
37
How do tissue metabolites affect vascular smooth muscle?
Tissue metabolites directly act on vascular smooth muscle to cause hyperpolarization and vasodilation.
38
What happens to potassium ion (K+) levels during increased metabolism?
Extracellular potassium levels (K+) increase due to potassium efflux from metabolizing cells.
39
How do potassium ions contribute to vasodilation?
Increased K+ opens potassium channels on smooth muscle cells, causing hyperpolarization and reduced calcium influx, leading to vasodilation.
40
What is the role of hydrogen peroxide (H₂O₂) in this process?
Increased H₂O₂ from metabolism contributes to opening potassium channels, promoting hyperpolarization and vasodilation.
41
What is the relationship between CO₂, H₂O, and HCO₃⁻ in smooth muscle?
CO₂ and H₂O are converted to HCO₃⁻ (bicarbonate) and H⁺, which can influence pH and smooth muscle relaxation.
42
What role does calcium (Ca²⁺) play in vascular tone?
Voltage-gated Ca²⁺ channels regulate calcium entry into smooth muscle cells, affecting contraction; hyperpolarization decreases Ca²⁺ influx, promoting relaxation.
43
How does the Na⁺/K⁺ pump contribute to smooth muscle function?
The pump helps maintain ionic balance by actively transporting 3 Na⁺ out and 2 K⁺ in, indirectly influencing hyperpolarization.
44
What metabolic changes lead to increased vasodilation?
Increased metabolism raises CO₂, H₂O₂, and extracellular K⁺, triggering mechanisms that open potassium channels and reduce calcium influx, leading to smooth muscle relaxation.
45
What is myogenic control in blood vessels?
It is the ability of smooth muscle in blood vessels to respond to changes in pressure or stretch to maintain consistent blood flow.
46
What triggers the activation of stretch-activated channels in vascular smooth muscle?
Increased stretch of the blood vessel wall.
47
What ion flows into the smooth muscle cell through stretch-activated channels during myogenic contraction?
Sodium (Na⁺).
48
What is the effect of sodium influx on the smooth muscle cell membrane?
Sodium influx causes membrane depolarization.
49
How does membrane depolarization lead to contraction in vascular smooth muscle?
Depolarization activates voltage-gated calcium (Ca²⁺) channels, allowing calcium influx, which triggers muscle contraction.
50
What is the role of calcium (Ca²⁺) in myogenic contraction?
Calcium binds to contractile proteins, initiating smooth muscle contraction.
51
How are adjacent smooth muscle cells coordinated during myogenic contraction?
Gap junctions allow the spread of electrical signals, coordinating contraction across cells.
52
What is flow autoregulation in blood vessels?
It is the process by which blood flow is maintained relatively constant despite changes in perfusion pressure.
53
Which two mechanisms are combined in flow autoregulation?
Myogenic control and metabolic control.
54
How does myogenic control contribute to flow autoregulation?
Myogenic control reduces blood flow in response to increased pressure by causing smooth muscle contraction.
55
How does metabolic control contribute to flow autoregulation?
Metabolic control increases blood flow in response to the accumulation of metabolites in active tissues.
56
What triggers myogenic contraction in response to increased perfusion pressure?
57
How does vessel size affect the relative importance of metabolic vs. myogenic regulation?
The importance of metabolic regulation increases as the diameter of resistance vessels decreases.
58
What triggers the release of nitric oxide (NO), prostacyclin, and EDHF from the endothelium?
Stimuli such as acetylcholine (from PNS nerves), bradykinin, histamine (autocoids), and flow-induced shear stress.
59
What is the role of nitric oxide (NO) in vascular control?
NO causes vasodilation by relaxing the smooth muscle.
60
Which molecule triggers the release of endothelin from the endothelium?
Angiotensin II.
61
Which molecules act on endothelial receptors to stimulate nitric oxide (NO) release?
Autocoids such as bradykinin and histamine.
62
How does laminar blood flow contribute to nitric oxide (NO) production?
Laminar flow creates shear forces sensed by mechanoreceptors on the endothelium, triggering NO release.
63
What enzyme is responsible for producing nitric oxide in the endothelium?
Endothelial nitric oxide synthase (eNOS).
64
What is the role of L-arginine in the production of nitric oxide?
L-arginine is the substrate used by eNOS to produce nitric oxide (NO).
65
What happens to intracellular calcium levels when autocoids bind to endothelial receptors?
Intracellular calcium levels increase, activating eNOS to produce nitric oxide.
66
What is the effect of nitric oxide (NO) on vascular smooth muscle?
NO diffuses to the smooth muscle, causing relaxation and vasodilation.
67
What triggers eNOS activation in endothelial cells?
Increased intracellular calcium, and shear stress from blood flow.
68
What is the initial action of nitric oxide (NO) on smooth muscle cells?
NO activates soluble guanylate cyclase (GC), converting GTP to cyclic GMP (cGMP).
69
How does cGMP mediate relaxation in smooth muscle?
cGMP activates protein kinase G (PKG), which reduces intracellular calcium levels and promotes relaxation.
70
What role do potassium (K⁺) channels play in NO-mediated smooth muscle relaxation?
K⁺ channels open, causing hyperpolarization of the membrane, which decreases calcium influx through voltage-gated calcium channels (VGCC).
71
What is the role of SERCA in smooth muscle relaxation?
SERCA (sarco/endoplasmic reticulum Ca²⁺ ATPase) pumps calcium into the sarcoplasmic reticulum, reducing cytosolic calcium levels.
72
What does PMCA do in the context of NO action on smooth muscle?
PMCA (plasma membrane Ca²⁺ ATPase) removes calcium from the cell, further lowering cytosolic calcium levels.
73
How does phosphodiesterase (PDE) affect cGMP levels?
PDE degrades cGMP into GMP, terminating its signaling effects.
74
What is the role of nitric oxide (NO) in resting (baseline) blood flow?
NO maintains baseline blood flow by counterbalancing the constrictor action of noradrenaline from sympathetic nerves and hormones like angiotensin II.
75
What happens to blood flow when an eNOS inhibitor like L-NMMA is used?
Blood flow decreases because NO production is blocked, reducing vasodilation.
76
whats the sequence of events during anaphylactic shock
77
What are the three major endothelium-derived factors involved in vascular control?
Prostacyclin (PGI₂), hyperpolarizing factors (EDHF), and endothelin.
78
What is the function of prostacyclin (PGI₂) in vascular regulation?
PGI₂ causes vasodilation by increasing cAMP levels in smooth muscle and also inhibits platelet aggregation (Stage 2 of clotting).
79
How do hyperpolarizing factors (EDHF) contribute to smooth muscle relaxation?
EDHF opens potassium (K⁺) channels, leading to membrane hyperpolarization and reduced calcium (Ca²⁺) influx, promoting vasodilation.
80
What is the role of endothelin in vascular tone?
Endothelin acts as a vasoconstrictor, increasing calcium levels in smooth muscle to promote contraction.
81
What triggers the release of vasodilating autocoids like prostacyclin and EDHF?
Flow-induced shear stress or the action of vasodilating autocoids on endothelial cells.
82
Which hormones can stimulate the release of endothelin?
Vasoconstrictor hormones like angiotensin II and thrombin.
83
What causes endothelial dysfunction in oxidative stress?
The overproduction of reactive oxygen species (ROS), such as superoxide and hydrogen peroxide, interferes with endothelial function.
84
Which cardiovascular risk factors are associated with oxidative stress?
Hypercholesterolemia, diabetes, smoking, and turbulent blood flow, all of which contribute to inflammation and oxidative stress.
85
What are the primary sources of superoxide (O₂⁻) in oxidative stress?
NADPH oxidase and mitochondria.
86
How does superoxide (O₂⁻) impact nitric oxide (NO)?
Superoxide reacts with nitric oxide, preventing NO-mediated vasodilation.
87
What is the consequence of oxidative stress on blood vessels?
Oxidative stress reduces the ability of blood vessels to dilate properly.
88
How is hydrogen peroxide (H₂O₂) formed in oxidative stress?
Superoxide (O₂⁻) is converted into hydrogen peroxide (H₂O₂).
89
Why is nitric oxide important in vascular health?
Nitric oxide mediates vasodilation, maintaining proper blood flow and vascular tone.
90
What percentage of resting cardiac output is directed to the heart?
4% of the resting cardiac output, which is 200 ml/min out of 5000 ml/min.
91
How does coronary blood flow change during moderate and intense exercise?
Moderate exercise: Increases to 400 ml/min.
Intense exercise: Increases to 800 ml/min.
92
How is coronary blood flow related to oxygen consumption?
There is a direct, proportional relationship between coronary blood flow and oxygen consumption.
93
What is the distribution of blood flow at rest for major organs?
94
What is the capillary density in the coronary circulation?
Approximately one capillary per myocyte.
95
How does the coronary circulation regulate blood flow at rest and during increased demand?
Flow autoregulation occurs at rest, and strong active hyperaemia is triggered when needed.
96
How does adrenaline affect coronary blood vessels?
Adrenaline acts as a coronary vasodilator via β₂ receptors.
97
When is the left ventricular myocardium perfused, and why?
Only during diastole, because intramyocardial arterioles are compressed during systole.
98
Under what conditions is the coronary circulation vulnerable to ischaemia?
When heart rate increases (diastole shortens more than systole).
When coronary arteries are narrowed by stenosis.
99
What is the resting metabolic demand of cardiac muscle as a percentage of cardiac output?
4% of cardiac output.
100
What triggers the mechanism of active hyperaemia in cardiac muscle?
Increased metabolic demand and increased cardiac output during activities like exercise or stress.
101
How does increased cardiac muscle work affect oxygen and metabolite levels?
It increases oxygen consumption and metabolite production.
102
Which 3 molecules contribute to coronary arteriolar dilation during active hyperaemia?
Adenosine: From ATP metabolism.
Potassium ions (K⁺): From repeated cardiac muscle repolarizations.
Carbon dioxide (CO₂): Increases, lowering pH (negative feedback loop).
103
What role does adrenaline play in active hyperaemia?
Adrenaline, acting on β₂ receptors, promotes coronary arteriolar dilation.
104
Why does coronary arteriolar dilation occur predominantly during diastole?
Because coronary vessels are compressed during systole, limiting perfusion.
105
How does the sympathetic nervous system contribute to active hyperaemia?
It activates the release of adrenaline and enhances vasodilation to meet increased metabolic demand.
106
What is the negative feedback mechanism in active hyperaemia?
Increased CO₂ and decreased pH regulate further metabolic and vascular responses to balance oxygen supply and demand.
107
What is required for coronary blood flow to occur?
Blood flow is driven by a **pressure difference** (p1 minus p2)
108
When is coronary blood flow at its lowest during the cardiac cycle?
During systole, when left ventricular arterioles are compressed.
109
When is coronary blood flow at its highest?
During early diastole, when the myocardium is relaxed, aortic pressure is high, and ΔP is maximal.
110
What happens to coronary blood flow during isovolumetric contraction?
Coronary blood flow falls to zero or may even briefly reverse because the contracting myocardium compresses the coronary arterioles.
111
How does coronary blood flow change during the ejection phase?
It briefly rises in line with aortic pressure.
112
Why does ΔP vary during the cardiac cycle?
It is lowest during systole due to ventricular compression.
It is highest during diastole when the myocardium relaxes.
113
What happens to ΔP after the aortic valve closes?
ΔP falls as aortic pressure decreases, and the myocardium remains contracted, limiting blood flow.
114
Why does coronary blood flow gradually decline during diastole?
The elastic energy in the aorta is depleted, reducing aortic pressure and ΔP
115
What is the relationship between aortic pressure and coronary blood flow during diastole?
High aortic pressure during diastole drives peak coronary blood flow.
116
What happens to heart rate during intense exercise?
Heart rate increases approximately threefold, from 70 beats/min at rest to 180 beats/min during intense exercise.
117
How does an increased heart rate affect diastole and perfusion time?
Diastole: Shortens significantly (from 0.5 seconds at rest to 0.13 seconds during exercise).
Perfusion time: Decreases (from 35 seconds/min at rest to 23 seconds/min during exercise).
118
How does cardiac output change during intense exercise?
Cardiac output increases fourfold, from 5 L/min at rest to 20 L/min during exercise.
119
How does mean coronary blood flow adjust to match cardiac output during exercise?
Mean coronary blood flow increases fourfold, from 200 ml/min at rest to 800 ml/min during exercise.
120
What enables coronary blood flow to increase despite shorter diastole?
Accumulated metabolites cause enhanced vasodilation during the shortened diastole, utilizing the coronary flow reserve.
121
Why does right coronary blood flow continue during systole?
Aortic pressure rises more than RV pressure during systole, maintaining a positive ΔP
122
How does right ventricular pressure (RV pressure) compare to left ventricular pressure (LV pressure) throughout the cardiac cycle?
RV pressure is much lower than LV pressure, allowing ΔP (pressure difference) to remain substantive throughout the cardiac cycle.
123
How does vessel compression differ between the right and left ventricles?
Compression of vessels in the wall of the right ventricle is negligible compared to the left ventricle.
124
What is the effect of systole on right coronary blood flow?
Blood flow is maintained during systole because the pressure gradient (ΔP) is sufficient.
125
Why must cerebral blood flow remain relatively constant?
To meet the brain's constant metabolic demand, even during intense physical activity, and to prevent neuronal damage or vascular injury.
126
What happens if there is not enough cerebral blood flow?
Neurons become starved of oxygen and quickly die.
127
What can occur if there is too much cerebral blood flow?
Cerebral vessels may rupture, leading to cerebral hemorrhage.
128
How is constant cerebral blood flow achieved despite changes elsewhere in the body?
Through **flow autoregulation** which adjusts cerebral vessel resistance to maintain steady blood flow.
129
How is cerebral blood flow maintained despite changes in perfusion pressure?
By adjusting vascular resistance through flow autoregulation.
130
What equation describes the relationship between flow, pressure, and resistance?
p = pressure
r = resistance
131
What happens to cerebral arterioles when perfusion pressure increases?
They constrict, reducing flow to maintain it at a normal level.
132
What happens to cerebral arterioles when perfusion pressure decreases?
They dilate, increasing flow to bring it back to normal.
133
What prevents cerebral haemorrhage during increased cardiac output or mean arterial pressure (MAP)?
134
What mechanism restores cerebral blood flow during haemorrhage-induced low perfusion pressure?
135
What triggers the mechanism of cerebral flow autoregulation?
Increased cardiac output (CO) and/or mean arterial pressure (MAP).
136
What happens to cerebral blood flow when CO or MAP increases?
Cerebral blood flow increases more than needed, leading to increased cerebral perfusion pressure.
137
How does the stretch of arterioles contribute to autoregulation?
Circumferential stretch of arterioles activates the myogenic response, causing arteriolar constriction.
138
How does excessive blood flow affect carbon dioxide levels in the brain?
CO2 is washed away faster than it is produced, leading to decreased CO2 levels in the blood.
139
How does reduced CO2 influence cerebral arterioles?
Reduced CO2 triggers a metabolic response, further contributing to arteriolar constriction.
140
What is the outcome of the combined myogenic and metabolic responses during autoregulation?
Cerebral blood flow is decreased back to normal levels, ensuring it matches the brain's metabolic demand.
141
What happens if CO or MAP is reduced, such as after blood loss?
The opposite occurs: arterioles dilate, increasing blood flow to maintain the brain's metabolic demands.
142
What type of feedback loop regulates cerebral blood flow?
A negative feedback loop ensures blood flow remains appropriate for the brain's metabolic needs.
143
What happens in a healthy coronary artery during rest?
large pressure drop across the vasculature supports sufficient blood flow, with partially constricted arterioles maintaining the capacity for increased flow during exercise.
144
How does stenosis affect coronary blood flow?
Stenosis introduces additional resistance, reducing the pressure drop across the microvessels and thereby reducing blood flow to the cardiac muscle.
145
What compensatory mechanism occurs in response to stenosis in coronary arteries?
Accumulated metabolites trigger vasodilation of the microvessels to restore flow, a process known as active hyperaemia.
146
What is coronary flow reserve, and how is it affected by stenosis?
Coronary flow reserve is the capacity to increase blood flow to meet metabolic demands. Severe stenosis depletes this reserve, as arterioles are maximally dilated at rest.
147
What risk is associated with a depleted coronary flow reserve due to stenosis?
The risk of heart attack increases during exercise as coronary arteries cannot meet the increased metabolic demand.
148
What 3 things is the microcirculation composed of?
Terminal arterioles, capillaries, and post-capillary venules.
149
What is the primary function of the microcirculation?
To exchange gases, water, nutrients, waste materials, and other substances between the blood and body tissues via the interstitial compartment.
150
What is the structure of the microcirculation?
It is a 3-D meshwork of blood vessels with diameters ranging from 3 to less than 10 microns.
151
What controls terminal arterioles?
Terminal arterioles are controlled by local factors and regulate flow through a set of capillaries.
152
What is unique about capillaries and post-capillary venules in terms of structure?
They contain no smooth muscle and serve as the primary exchange vessels
153
What is the role of lymphatic capillaries in the microcirculation?
They take up fluid and protein, return them to the blood, and transport microorganisms to lymph glands.
154
