Feb 26 - Arteries and Arterioles

Question 1

What is another name that describes arteries?

Answer 1

Conductance vessels

Question 2

What is another name that describes arterioles?

Answer 2

Resistance vessels

Question 3

What is another name that describes veins?

Answer 3

Capacitance vessels

Question 4

What components are included in arteries?

Answer 4

Smooth muscle cells (regulate vessel diameter)
Endothelial cells (regulate smooth muscle function, vessel permeability)
Collagen fibres (impart rigidity to the arterial wall)
Elastic laminae (impart elasticity to the arterial wall)

Question 5

What is the role of arteries?

Answer 5

Arteries are specialized structures that serve as conduits for the movement of blood from the heart to the other tissues. They offer little resistance to flow due to their relatively large diameter. Negligible loss of energy occurs down the arterial tree (approx 4 mmHg), and arterial pressure is essentially the same throughout the system (little resistance to flow). Arteries can act as a pressure reservoir for forcing blood movement when the heart relaxes (storage of potential energy)

Question 6

Blood pressure is a function of what?

Answer 6

Blood pressure is a function of the volume of blood in the vessel, and the compliance (distensibility) of the vessel

Question 7

How does the amount of blood entering/leaving a vessel affect the pressure gradient?

Answer 7

Consider the aorta: it is high distensible, and receives a large bolus of blood on each cardiac contraction. If the volume of blood entering the vessel (Vin) is equal to the volume of blood leaving the vessel (Vout), then there is no change in the pressure exerted by the blood on the walls of the vessel. During systole: Vin>Vout, therefore the pressure increases - vessel wall expands. During diastole: Vin<Vout, therefore the pressure gradient decreases - vessel wall contracts.

Question 8

How do the elastic properties of the arteries aid in the flow of blood?

Answer 8

The elastic properties of the arteries allow them to expand and thus store potential energy as blood volume increases with contraction. This energy is released in passive recoil of the arterial wall, which pushes blood downstream. As a result, downstream flow is “smoothed out”. Capillary blood flow is not intermittent, and does not parallel the contraction/relaxation cycle of the heart

Question 9

What gives the arteries their elastic properties?

Answer 9

These properties are imparted by a specific protein: elastin. The entropy of beta-coils in the amino acid sequence is maximal in non-stretched elastin molecules

Question 10

What are arterioles?

Answer 10

Arterioles are the major resistance vessels of the vascular tree

Question 11

Describe the pressure gradient of the arterioles

Answer 11

As blood flows through these vessels, the mean pressure falls from around 93 mmHg (mean arterial pressure) to 37 mmHg (pressure at the beginning of the capillaries

Question 12

Why is arteriolar resistance important?

Answer 12

Arteriolar resistance creates the pressure differential which encourages blood to flow from the heart to various organs downstream. This resistance also converts pulsatile pressure swings to nonfluctuating pressure in the capillaries. Each organ has a complement of arterioles that can be adjusted independently to determine the distribution of cardiac output and to regulate blood pressure

Question 13

Do arterioles have a lot of connective tissue?

Answer 13

No, arterioles have little connective tissue, but a relatively thick layer of smooth muscle

Question 14

Is blood evenly distributed evenly throughout the circulatory system?

Answer 14

No. Blood is not evenly distributed through the circulatory system; different vascular beds receive different amounts of blood (measured as percentage of cardiac output) and the amount that each bed receives will change depending on the metabolic needs of the tissue

Question 15

How does fluctuation of blood supply to different organs occur?

Answer 15

Any alteration in the total peripheral resistance will influence the mean arterial pressure immensely (upstream of the point of resistance). If all arteriolar beds opened maximally and simultaneously, blood pressure would drop substantially

Question 16

How is the total peripheral resistance (the radius) of arterioles controlled?

Answer 16

When arteriolar smooth muscle contracts, the vessel’s radius becomes smaller. As resistance is increased (due to vasoconstriction), blood flow is decreased. Regulation of arteriorlar diameter results in regulation of blood pressure and flow to the tissue or organ perfused by the arteriole. More blood flows to areas whose arterioles offer the lease resistance

Question 17

What is vasoconstriction?

Answer 17

Reduction of arteriorlar circumference due to contraction of smooth muscle lining the vessel

Question 18

What is vasodilation?

Answer 18

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

Question 19

What is vascular tone?

Answer 19

Partial constriction of the arteriole. Normally, some tone is present. Vascular tone allows for fine control of resistance (vasodilation and vasoconstriction). If tone did not exist, there would be no vasodilatory control

Question 20

How is vascular tone generated?

Answer 20

Myogenic activity - smooth muscle cell resting membrane potential can fluctuate, therefore self-induced contractile activity can occur. Continual release of norepinephrine form sympathetic fibres innervating the VSMCs, contributing to enhanced vascular tone

Question 21

What triggers vasconstriction?

Answer 21

Increase in myogenic activity (intrinsic)
Increase in oxygen (intrinsic)
Decrease in carbon dioxide and other metabolites (intrinsic)
Increase in sympathetic stimulation (extrinsic)
Vasopressin, angiotensin II (extrinsic)
Cold (intrinsic)

Question 22

What triggers vasodilation?

Answer 22

Decrease in myogenic activity (intrinsic)
Decrease in oxygen (intrinsic)
Increase in carbon dioxide and other metabolites (intrinsic)
Decrease in sympathetic stimulation (extrinsic)
Histamine release (extrinsic)
Heat (intrinsic)

Question 23

How do intrinsic and extrinsic factors control arteriolar radius?

Answer 23

The amount of perfusion (i.e. blood flow) that a tissue receives is dependent upon many local (intrinsic) and systemic (extrinsic) factors, which together determine the amount of vasoconstriction/vasodilation that occurs; these factors may be physical or chemical and ultimately work by changing the amount of contraction of the smooth muscle cells lining the arteriole

Question 24

How do local factors and systemic factors interact?

Answer 24

Local/intrinsic factors can either reinforce the sytemic signals, or oppose them. Local factors are restricted to a specific vascular bed, regulating net blood flow to the tissue. Local intrinsic arteriolar adjustments override systemic extrinsic effects

Question 25

What are important extrinsic factors for control arteriolar resistance?

Answer 25

Neural and hormonal, with the effects of the sympathetic nerves being the most important

Question 26

How does sympathetic control regulate arteriolar radius?

Answer 26

Sympathetic nerve fibres, descending from the CV control centre of the brain, supply all the smooth muscle except that in the brain. Vascular tone is maintained by a basal level of sympathetic activity, which generally causes vasoconstriction. Elevated sympathetic activity results in arteriolar vasoconstriction. Decreased sympathetic activity results in arteriolar vasodilation. Overall sympathetic activation can greatly increase blood pressure by increasing cardiac output and TPR concurrently

Question 27

What are autonomic reflexes?

Answer 27

A number of autonomic reflexes (e.g., baroreceptors, chemoreceptors, low-pressure receptors, etc.) exist to maintain blood pressure within specific biological limits

Question 28

What is a vasodilator hormone?

Answer 28

Bradykinin is a substance that lasts only for a few minutes in the circulation but causes powerful dilation and increased capillary permeability

Question 29

What is are vasoconstrictor hormones?

Answer 29

Norepinephrine and epinephrine
Angiotensin II
Vasopressin

Question 30

How do norepinephrine and epinephrine work to cause vasoconstriction?

Answer 30

Norepinephrine and epinephrine are potent vasoconstrictors released from the adrenal medullae directly into the blood to promote systemic vasoconstriction and increased blood pressure. This vasoconstrictor effect is typically mediated by alpha-1 adrenoceptors. However, epinephrine also binds to beta-2 adrenoceptors to cause vasodilation in tissues with an abundance of these receptors (i.e. heart and skeletal muscle

Question 31

How does angiotensin II work to cause vasoconstriction?

Answer 31

Angiotensin II is another powerful vasoconstrictor. It acts to increase TPR and therefore blood pressure. As a result,this hormone contributes to the development of hypertension in many pathological CV conditions. At the local level, angiotensin II can severely limit blood flow by promoting severe vasoconstriction

Question 32

How does vasopressin work to cause vasoconstriction?

Answer 32

Vasopressin (aka antidiuretic hormone) is an even more potent vasoconstrictor than angiotensin II. It is 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

Question 33

What are important intrinsic factors for control of arteriolar radius?

Answer 33

Local controls can either be chemical or physical in nature

Question 34

How do oxygen and carbon dioxide levels work as chemical regulators of arteriolar radius?

Answer 34

High oxygen tension (low carbon dioxide) causes vasoconstriction
High carbon dioxide tension (low oxygen) causes vasodilation

Question 35

How does low oxygen/high carbone dioxide cause vasodilation?

Answer 35

Oxygen is required for oxidative phosphorylation (ATP production), which in turn is required for smooth muscle contraction, i.e. to maintain vascular tone. When metabolic demands increase, oxygen is depleted; as a result, muscle tension cannot be maintained, the vessel dilates and flow to the tissues increases.

Question 36

What is active hyperemia?

Answer 36

A phenomenon in which there is an increase in blood flow in order to meet increased local metabolic demand

Question 37

What are some vasodilator produced by metabolizing tissues (besides carbon dioxide)?

Answer 37

Acids (H+ and lactate, which lower pH), potassium ions (due to the increased number of action potentials) and adenosine (from the breakdown of high energy phosphates). Increased blood flow will assist with the removal of these substances

Question 38

Describe the control of arteriolar radius offered by prostaglandins

Answer 38

Lipid-derived prostaglandins can behave as vasodilators and are produced by many cell types, often as part of the inflammatory response. Many pain-killers and anti-inflammatories (e.g., aspirin) antagonize the prostaglandin pathway

Question 39

Describe the control of arteriolar radius offered by histamine

Answer 39

Histamine is another local chemical modulator that causes vasodilation of arteriolar smooth muscle, but is usually only released upon mechanical damage to tissues or during an allergic reaction; histamine arises from connective tissue cells or circulating white blood cells

Question 40

Endothelial cells lining the arteries and arterioles are capable of producing a number of vasoactive substances including what?

Answer 40

EDRF
EDHF
Endothelin

Question 41

How does EDRF work to control arteriolar radius?

Answer 41

EDRF, or endothelial-derived relaxing factor, is a potent vasodilator that has been identified as the solube gas nitric oxide (NO). NO diffuses to neighboring smooth muscle and induces relaxation. Impaired NO production has been associated with hypertensive disorders

Question 42

How does EDHF work to control arteriolar radius?

Answer 42

EDHF, or endothelial-derived hyperpolarizing factor, is a vasodilator substance (or phenomenon) that to date remains unidentified. EDHF may play a key anti-hypertensive role specifically in females, and its identity may vary depending on the specific vascular bed

Question 43

How does endothelin work to control arteriolar radius?

Answer 43

Endothelin is a 21 amino acid peptide present in endothelial cells of most blood vessels. It can be released in response to vascular damage caused by physical trauma. It stimulates severe vasoconstriction to help prevent extensive bleeding from arteries larger than 5 mm in diameter that may have been torn open

Question 44

How does heat and cold act as physical regulators of arteriolar radius?

Answer 44

Heat increases blood flow; cold decreases blood flow (a cold compress helps relieve the swelling of an inflammatory response - the cold causes vasoconstriction, resulting in reduced blood flow into the affected tissue)

Question 45

How does myogenic response to stretch act as a physical regulator of arteriolar radius?

Answer 45

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. These responses, in combination with effects of metabolites, are important in reactive hyperemia and pressure autoregulation

Question 46

How does reactive hyperemia act as a physical regulator of arteriolar radius?

Answer 46

When blood flow to a tissue is totally restricted, myogenic relaxation is coupled with a decrease in oxygen levels (and increased metabolites) in that tissue. The result is a large but transient increase in blood flow once the occlusion is removed

Question 47

How does shear stress act as a physical regulator of arteriolar radius?

Answer 47

A longitudinal force induced by the friction of blood flowing over the endothelial cell surface (increased blood flow will result in increased shear). As a result, these cells release the potent vasodilator nitric oxide (NO), causing relaxation of underlying smooth muscle

Question 48

What is pressure autoregulation?

Answer 48

A means by which tissues resist changes in blood flow, in the face of changes in mean arterial pressure

Question 49

How does pressure autoregulation work when there is a drop in MAP (e.g., hemorrhage)

Answer 49

A drop in MAP 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

Question 50

How does pressure autoregulation work when there is an increase in MAP (e.g., hypertension)?

Answer 50

Increased MAP leads to increased blood flow and increased stretch of arterioles, resulting in reflex vasoconstriction to restore blood flow back to normal. Increased NO release due to increased shear force is likely also involved

Question 51

Exercise is an example of a situation where blood flow changes dramatically and quickly. Explain

Answer 51

In working skeletal muscles, greatly increased local metabolic demand results in vasodilation which, combined with increased cardiac output, leads to a major increase in local blood flow. At the same time, blood flow to the kidneys and digestive tract is reduced due to vasoconstriction in these organs. In contrast, blood flow to the brain never varies with exercise or sleep, although changes in local activity do affect regional distribution and flow within the brain itself.

Question 52

Skeletal muscle and cardiac muscle have powerful local control mechanisms to override generalized sympathetic vasoconstriction, as well as local beta-2 adrenoceptors to promote vasodilation. Explain how this works upon starting exercising (i.e. pedaling a bike)

Answer 52

Sympathetic drive is increased throughout the body, resulting in generalized vasoconstriction. At the same time, localized control mechanims (e.g., active hyperemia) override the vasoconstrictor effects and cause vasodilation in the exercising muscles (i.e. the legs). The net result is that blood is directed away from tissue beds such as the GI tract and towards the exercising muscle. Note that non-exercising muscles (e.g., the arm) will not have the local controls activated, therefore flow will be reduced to the non-exercising muscles as well