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Physiology > Lecture 13: Local and Humoral control of blood flow > Flashcards

Lecture 13: Local and Humoral control of blood flow Flashcards

1
Q

How is blood distributed throughout the circulatory system?

A

Different vascular beds receive different amounts of blood (measured as a percentage of cardiac output)

depends on the normal metabolic needs of the tissue.

See figure

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2
Q

Variations in blood flow to different organs

A

Some organs tend to receive much more blood than they typically need, and can survive large fluctuations in blood flow without damage.

Other organs including brain and heart (equipped almost solely for aerobic respiration) are sensitive to changes in blood flow, and are easily damaged by insufficient flow

Blood flow to the kidneys, skin and digestive organs may change drastically in the course of normal physiology (i.e. exercise).

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3
Q

What physical factors determine blood flow?

A

Pressure

Resistance

CO = MAP/TPR

Flow = delta P/ Resistance

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4
Q

What is the main driving force for flow through a vessel?

A

Pressure gradient (delta P)

**it is the difference in pressure, NOT the absolute pressure that is critical

See figure

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5
Q

What forces are responsible for resistance to flow?

A

Friction from the blood rubbing against vessel wall

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6
Q

Relationship of resistance to vessel surface area

A

Greater vessel surface area in contact with blood (small diameter arteriole) causes greater resistance to flow

Energy is lost as blood moves from great arteries through the arteriolar network

See figure

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7
Q

Relationship of resistance to vessel radius and flow

A

Resistance is inversely related to the fourth power of vessel radius (r)

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8
Q

What would happen to resistance if arteriolar radius increased by 2x? What would happen to flow rate?

A

16 fold decrease in resistance

16 fold increase in flow rate (flow rate is inversely related to resistance)

See figure

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9
Q

What is Poseuille’s law?

A

Describes the factors that affect flow rate through a vessel

See figure

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10
Q

Which component of poseuille’s law has the largest and most important contribution to resistance?

A

Radius of the vessel

Actively regulated

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11
Q

What is atheroscleorosis?

A

Radius narrows due to plaque

In order to maintain flow, the heart must work harder

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12
Q

Where is pressure lost in the circulatory system?

A

Mostly in arterioles

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13
Q

Comparison of blood vessels

A

See table

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14
Q

Which vessels are the major resistance vessels of the vascular tree?

A

Arterioles

As blood flows through these vessels, the mean pressure falls from ~93 mm Hg (i.e. mean arterial pressure) to 37 mm Hg (pressure at the beginning of capillaries).

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15
Q

What does arteriolar resistance create?

A

the pressure differential which encourages blood to flow from the heart to various organs downstream.

also converts pulsatile pressure swings to non-fluctuating pressure in the capillaries.

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16
Q

Role of arterioles in organs

A

Each organ has a complement of arterioles that can be adjusted independently to determine the distribution of cardiac output and to regulate blood pressure.

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17
Q

Arteriolar wall composition

A

little connective tissue

relatively thick layer of smooth muscle allowing for robust contraction.

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18
Q

Regulation of arteriolar diameter

A

Any alteration in the resistance (TPR) will influence the mean arterial pressure upstream of the point of resistance

If all arteriolar beds open maximally all at once = blood pressure drops

See figure

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19
Q

How is tissue blood flow regulated?

A

Regulation of arteriolar diameter results in regulation

More blood flows to areas whose arterioles offer the least resistance to its passage

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20
Q

What is vasoconstriction?

A

Reduction of arteriolar circumference due to contraction of smooth muscle lining the vessel.

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21
Q

What is vasodilation?

A

Enlargement of the circumference and radius of a vessel due to relaxation of smooth muscle.

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22
Q

What is vascular tone? What does it allow?

A

Partial constriction of the arteriole. Normally, some tone is present.

Vascular tone allows for fine control of resistance (vasodilation and vasoconstriction).

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23
Q

What would happen if tone did not exist?

A

No vasodilatory control

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24
Q

Structure of the circulatory system in local tissues

A

Conduit artery

Feed artery

Primary arteriole

Terminal arteriole

Capillary

Capillary

Venule

Vein

See figure

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25
Q

Role of conduit arteries

A

Designed to transport blood to areas of the body

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26
Q

Role of feed arteries

A

Vascular resistance vessels designed to regulate flow to specific areas of the body.

account for ~ 50% of TPR.

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27
Q

Role of terminal arterioles

A

last control point for regulating blood flow into capillaries.

Therefore, to
perfuse a microvascular unit, the terminal arteriole must be dilated.

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28
Q

What is an MVU?

A

Microvascular unit

all of the capillaries arising from a common terminal arteriole

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29
Q

Role of capillaries

A

Capillaries are considered to be the primary location
where oxygen transfer occurs in muscle.

There is no VSM in capillaries, rather there is only an endothelial layer.

This promotes diffusion by limiting the distance that oxygen must diffuse.

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30
Q

Which vessels are surrounded by SNS nerves? Role?

A

The feed arteries and arterioles

may activate vasoconstriction to increase systemic TPR to enhance blood pressure and to limit blood flow to areas of low metabolic demand.

Veins, but not venules are surrounded by SNS nerves

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31
Q

How may venules become constricted?

A

spillover from the arterioles may constrict venules to promote venous return.

This type
of control is not as important as the control of vasoconstriction of arterioles because veins
are very elastic and can
stretch to accommodate
more volume
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32
Q

How does vasodilation migrate in response to metabolic accumulation?

A

Distal to proximal vessels

Step 1. Metabolic accumulation is sensed by the capillaries and terminal arterioles, which triggers local vasodilation as well as upstream vasodilatation of the terminal arterioles.

Step 2. GAP junctions within the endothelium and VSMC send a signal up the arterial tree to vasodilate primary
arterioles and feed arteries.

This is particularly important Because feed arteries are not located in muscle and
are not exposed to metabolic stimuli.

Step 3. Conduit arteries are located outside of muscle and therefore are physically removed from the local metabolite and vasoactive stimuli produced by skeletal muscle.

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33
Q

Why does vasodilation ascend from distal to proximal vessels? Why not dilate upstream feed arteries to perfuse all the vessels downstream?

A

It does this so that the system is able to specifically match perfusion of local tissues with the metabolic demand of the specific tissue.

Thus, the system optimizes local blood flow by making sure the system is able to accommodate and needs the added blood flow without sacrificing blood flow to other parts of the body

See figure

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34
Q

What causes arteriolar vasoconstriction

A

Increased myogenic activity

Increased O2

Decreased CO2 and other metabolites

Increased SNS stimulation, vasopressin, angiotension II, cold

See figure

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35
Q

What causes arteriolar vasodilation?

A

Decreased myogenic activity

Decreased O2

Increased CO2 and other metabolites

Decreases SNS stimulation, histamine, heat

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36
Q

Systemic/extrinsic factors vs local/intrinsic factors

A

Systemic factors affect arterioles throughout the body (exception: brain). Regulate systemic blood pressure

Local factors either reinforce or oppose systemic factors. Restricted to specific vascular bed. Regulate net flow to the tissue

LOCAL OVERRIDES SYSTEMIC

See figure

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37
Q

What is extrinsic control of arteriolar resistance important for?

A

important in overall regulation of arterial blood pressure.

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38
Q

What are the important factors for extrinsic control of arteriolar resistance?

A

Neural and hormonal factors

Effects of SNS nerves are most important

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39
Q

What do sympathetic nerve fibres supply?

A

descend from the cardiovascular control centre of the brain

supply all smooth muscle except that in brain tissue.

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40
Q

How is vascular tone maintained?

A

maintained by a basal level of sympathetic activity, which generally causes vasoconstriction.

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41
Q

What does elevated SNS activity cause to arterioles? Decreased SNS?

A

Elevated SNS = arteriolar vasoconstriction

Decreased SNS = arteriolar vasodilation

42
Q

How does SNS activation cause big increase in MAP?

A

sympathetic activation of the heart results in increased contractility and heart rate

overall sympathetic activation thus can greatly increase blood pressure by increasing cardiac output and total peripheral resistance

43
Q

Central regulation of pressure/resistance/output

A

Central command

Arterial baroreflex

Skeletal muscle afferents

See figure

44
Q

What is central command?

A

A feed forward system

volitional activity can influence cardiovascular responses.

The activation of the motor cortex can influence the regulation of PNS and SNS systems, thereby affecting cardiovascular regulation.

45
Q

What is the arterial baroreflex?

A

Baroreceptors are pressure-sensitive receptors located in the carotid sinus (neck) and the aortic arch (immediately after the heart) .

These receptors are activated in response to high or low blood pressures and act to rapidly regulate blood pressure on a beat to beat basis.

Upon activation, baroreceptors can influence the PNS and SNS systems.

46
Q

Skeletal muscle afferents

A

Mechanoreceptors/ metabaroreceptors

located in muscle and sense mechanical or metabolic signals associated with muscle contraction.

Upon activation, these receptors primarily influence the SNS system to increase blood pressure and HR.

These receptors contribute to the central control of blood flow.

47
Q

What type of control do vasoconstrictor hormones have on arteriolar diameter? What are these hormones?

A

Extrinsic regulation

Norepinephrine

Epinephrine

Angiotensin II

Vasopressin

Serotonin and thomboxane A2

48
Q

Where are norepinephrine and epinephrine secreted from? Role?

A

Potent vasoconstrictors released from the adrenal medullae directly into the blood

Promote systemic vasoconstriction and increased blood pressure.

49
Q

Angiotensin II role

A

Acts to increase total peripheral resistance and therefore blood pressure.

At the local level, angiotensin II can severely limit blood flow by promoting severe vasoconstriction.

50
Q

Pathological role of angiotensin II

A

Contributes to the development of hypertension in many pathological cardiovascular conditions.

51
Q

Vasopressin role, formation and storage?

A

(also called antidiuretic hormone)

even more potent vasoconstrictor than Angiotensin II

Formed in nerve cells in the hypothalamus and is stored in the posterior pituitary gland.

When secreted into the blood, it can influence blood pressure regulation during severe hemorrhage.

However, it is not clear if vasopressin has a role in the regulation of blood pressure during physiological conditions.

52
Q

When are serotonin and thromboxane A2 released?

A

released from platelets during vascular injury.

53
Q

What are the vasodilator hormones? What type of regulation do they exert on arteriolar diameter?

A

Bradykinin

Histamine

Extrinsic regulation

54
Q

What is bradykinin?

A

lasts only for a few minutes in the circulation

causes powerful dilation and increased capillary permeability.

55
Q

What is histamine? Where does it come from?

A

local chemical modulator that causes vasodilation of arteriolar smooth muscle

usually only released upon mechanical damage to tissues or during an allergic reaction

histamine arises from connective tissue cells or circulating white blood cells.

56
Q

What is the role of intrinsic control of arteriolar diameter?

A

Match blood flow to a specific tissue’s metabolic needs

Important for adjusting cardiac output to the organ’s needs (fraction of cardiac output for each organ is altered depending on metabolic requirements)

57
Q

Nature of local controls of arteriolar diameter

A

Chemical or physical

58
Q

Chemical intrinsic regulators of arteriolar diameter

A

High O2 tension (low CO2) = vasocontriction

High CO2 tension (low O2) = vasodilation

Other metabolites

Prostaglandins

Prostacyclin

EDRF

EDHF

Endothelin

59
Q

What is active hyperaemia?

A

Oxygen is required for oxidative phosphorylation (ATP production)

ATP is required for smooth muscle contraction

When metabolic demands increase, O2 is depleted and muscle tension cannot be maintained, vessel dilates and flow to tissue increases

60
Q

Products of actively metabolizing tissues in arteriolar diameter regulation

A

Intrinsic control

Produce CO2, acids (H+ and lactate, which lower pH), K+ (due to increased number of action potentials) and adenosine (from the breakdown of high energy phosphates

all of these substances are vasodilators

61
Q

How are metabolic products removed from vessels?

A

They cause vasodilation, which increases blood flow and washes away substances

62
Q

Role of prostaglandins in arteriolar diameter? Produced by? Antagonized by?

A

Chemical intrinsic regulator

Vasodilation

Produced by many cell types, often as part of inflammatory response

Antagonized by many pain killers and anti-inflammatories

63
Q

Role of prostacyclin in arteriolar diameter? produced by?

A

Chemical intrinsic regulator

Maintain normal flow

Produced by endothelial cells

64
Q

Vasoactive substances produced by endothelial cells

A

Chemical, intrinsic regulators

EDRF

EDHF

Endothelin

Released by endothelial cells but act on vascular smooth muscle

65
Q

EDRF - role, identity

A

Chemical, intrinsic

endothelial-derived relaxing factor

potent vasodilator that has been identified as the soluble gas nitric oxide (NO).

NO diffuses to neighboring smooth muscle and induces relaxation.

66
Q

What is impaired EDRF (NO) production associated with?

A

hypertensive disorders.

67
Q

EDHF - role, identity

A

Chemical, intrinsic

endothelial-derived hyperpolarizing factor

vasodilator substance (or phenomenon) that to date remains unidentified.

may play a key anti-hypertensive role specifically in females

its identity may vary depending on the specific vascular bed.

68
Q

Endothelin - structure, role

A

Chemical, intrinsic

21 amino acid peptide

Present in endothelial cells of most blood vessels

Can be released in response to vascular damage caused by physical trauma.

Stimulates severe vasoconstriction to help prevent extensive bleeding from arteries larger than 5 mm in diameter that may have been torn open.

69
Q

Histology of arterioles

A

See figure

70
Q

How NO release from endothelial cells is stimulated

A

As red blood cells bump into the epithelial cells, they cause the epithelial cells to deform, which triggers the release of nitric oxide.

Nitric oxide then signals the VSMC to relax, thereby enhancing local blood flow.

Nitric oxide also enhances the dilation of upstream terminal and primary arterioles to further increase local blood flow.

See figure

71
Q

Synthesis of NO

A

Synthesized from L-arginine by endothelial nitric oxide synthase (eNOS)

72
Q

What happens to NO in diseased states?

A

nitric oxide bioavailability is reduced due to an accumulation of oxidative stress

Excess oxygen free radicals combine with NO to create ONOO which damages cellular proteins

Less NO available, so impaired VSMC relaxation

= Vasodilation is impaired

See figure

73
Q

What is nitric oxide bioavailability?

A

the total amount of nitric oxide that is biologically active

the difference (mathematical function) between the total production of nitric oxide minus the total amount of nitric oxide destroyed by other processes

74
Q

Examples of pathological conditions that reduce NO bioavailability

A

Hypercholestrolemia

Atherosclerosis

Peripheral artery disease

Coronary artery disease

75
Q

What factors may enhance endothelial function and promote increase in NO bioavailability?

A

Exercise training

Medical treatments

76
Q

How does exercise increase NO bioavailability?

A

Increases eNos protein expression

Reduces the amount of ROS made by NADPH oxidase

Lower oxygen radicals lowers amount of -ONOO produced, which lowers cellular damage

May enhance Superoxide dismutase protein expression, which reduces oxidative stress

77
Q

How does SOD reduce oxidative stress?

A

Converts oxygen radicals into hydrogen peroxide (H2O2)

Catalase or glutathione peroxidase then converts H2O2 into water

78
Q

Physical, intrinsic regulators of arteriolar diameter

A

Heat, cold

Myogenic response

Shear stress

Pressure

79
Q

How do heat and cold regulate arteriolar diameter?

A

Physical, intrinsic

Heat increases bloodflow

Cold decreases blood flow (relieves swelling of inflammatory response)

80
Q

How does the myogenic response to stretch regulate arteriolar diameter?

A

VSMC responds to being passively stretched by increasing its tone.

Passive stretch is a function of the volume of blood delivered to an organ.

The converse is also true: reduction in blood flow to the tissue reduces passive stretch, resulting in decreased tone.

81
Q

What intrinsic responses are important in reactive hyperaemia and pressure auto regulation?

A

Myogenic response to stretch

Effects of metabolites

82
Q

What is reactive hyperaemia?

A

physical, intrinsic regulator

when blood flow to a tissue is totally restricted, myogenic relaxation is coupled with a decrease in O2 levels (and increased metabolites) in that tissue.

Result is a large but transient increase in blood flow once the occlusion is removed.

83
Q

What is shear stress?

A

physical, intrinsic regulator

a longitudinal force induced by the friction of blood flowing over the endothelial cell surface

As a result, these cells release the potent vasodilator nitric oxide (NO), causing relaxation of underlying smooth muscle.

84
Q

What is pressure autoregulation during a drop in MAP?

A

Physical, intrinsic regulator

a drop in MAP (e.g. hemorrhage) reduces blood flow and stretching of the arterioles, and metabolites build up

arterioles dilate to restore blood flow to the tissue, thus maintaining blood flow fairly constant.

85
Q

What is pressure autoregulation during an increase in MAP?

A

increased MAP (e.g. hypertension) leads to increased blood flow and increased stretch of arterioles

results in reflex vasoconstriction to restore blood flow back to normal.

Increased NO release due to increased shear force is likely also involved.

86
Q

Factors limiting maximal blood flow to tissues

A

1) The heart has a limit for the maximal amount of blood that it can pump each minute (maximal cardiac output).
2) There is a limited amount of total blood volume within the circulatory system that must perfuse a lot of different tissues.
3) There is a limited density of capillaries in each different type of tissue, which directly limits the perfusion of that tissue.

87
Q

Degree of perfusion of tissues at any given time depends on///

A

Systemic and local factors

Factors are tuned to different stimuli and drive specific responses (vasoconstriction of vasodilation)

88
Q

Are tissue metabolic demands static?

A

No

Can change rapidly

Results in need to quickly alter perfusion, often to many tissues at once.

This occurs automatically as the various systemic and local factors change.

89
Q

Distribution of cardiac output at rest vs exercise

A

See figure

90
Q

Tissue blood flow during exercise

A

During maximal muscle activity, flow undergoes a 20x increase. Cardiac output only undergoes a 5x increase.

Cardiac output does not dully account for the increased blood flow through the muscles

Second level of blood flow regulation is required. Circulatory system controls blood flow to local tissues as a way to optimize and match tissue perfusion with metabolic demand

91
Q

Effects of exercise on cardiovascular function

A

Increased CO (Increased HR, Increased SV)

Increased HR (Decreased PSNS singling - decreased vagal nerve stimulation, Increased SNS signalling)

Increased SV (Increased filling due to venous return, Increased contractility - frank starling)

Increased BP (Increased cardiac output, Increased systemic TPR)

See figure

92
Q

Vasodilation and vasoconstriction during maximal exercise

A

BP increases due to increase in TPR across entire system

Vasoconstriction in non-metabolically active tissue limits flow to tissue, allowing more blood to be directed to where the body needs it

Local control factors in metabolically active tissue vasodilator the local arterioles and enhance blood flow to this tissue

93
Q

Effect of number of capillaries on oxygen delivery

A

Each capillary supplies oxygen to a cylindrical region of surrounding tissue (Krogh cylinder)

The ability of the circulation to deliver oxygen to the tissue is thus directly related to the capillary density in the tissue.

94
Q

How can a person increase their capillary density?

A

Training their muscles

95
Q

What is involved in long term regulation of flow?

A

Vascularity

physical growth of new arterioles, capillaries and veins contributes to the long term regulation of blood flow to metabolically active tissue.

96
Q

Types of muscle fibres and capillary density

A

Oxidative fibres (Type 1 fibres) have a higher capillary density compared to glycolytic fibres (Type 2 fibres).

Endurance trained people have significantly more capillaries compared to sedentary people.

LACK OF OXYGEN IS MAJOR FACTOR IN THE GROWTH OF NEW CAPILLARIES

97
Q

Speed of capillary growth depending on situation

A

begins within days in extremely young animals

In new growth tissue (such as scars and cancerous tissue)

much more slowly in aged people or established tissue.

98
Q

Vascular growth factors

A

All are small growth factors

Vascular endothelial growth factor (VEGF)

Fibroblast growth factor (FGF)

Platelet-derived growth factor (PDGF)

Angiogenin

99
Q

What is reduced oxygen’s effect on gene expression?

A

Reduced oxygen tension can drive the expression of specific genes via oxygen- responsive transcription factors such as hypoxia-inducible factor 1α (HIF-1α)

100
Q

What is angiogenesis?

A

Growth of vessels

source of new cells is endothelial cells of existing vessels.

Grows directly off existing vessel

See figure

101
Q

What is vasculogenesis

A

Growth of vessels

source of precursor cells is the undifferentiated cells of the splanchnic mesoderm.

Grows spontaneously near the vessel then hooks onto it

Physiology (19 decks)

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