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PHYSIOLOGY II > WEEK VIII (Arterioles) > Flashcards

WEEK VIII (Arterioles) Flashcards

1
Q

_____________ are the major resistance vessels

A

Arterioles

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2
Q

Describe how blood flows from arterioles to the organs downstream

A

Arterioles have a SMALLER RADIUS compared to capillaries, resulting in significant RESISTANCE to flow -> High degree of ARTERIOLAR RESISTANCE leads to a significant DROP in MEAN PRESSURE as blood flows through ARTERIOLES and CAPILLARIES -> Pressure decline establishes a PRESSURE DIFFERENTIAL that promotes blood flow from the heart to the organs downstream

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3
Q

What does Arteriolar resistance do?

A
  • Leads to a significant drop in mean pressure as blood flows through arterioles and capillaries
  • Converts systolic-to-diastolic pressure swings in arteries into a STEADY PRESSURE in capillaries
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4
Q

The radius of arterioles supplying individual organs can be independently adjusted to accomplish which functions?

A
  • Distributing cardiac output Amongst organs based on the body’s needs
  • Helping regulate arterial blood pressure
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5
Q

Arterioles are innervated by which nerves?

A

Sympathetic nerve fibers

[except in the brain]

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6
Q

Describe Vasoconstriction and Vasodilation in arterioles

A

VASOCONSTRICTION = Occurs when the smooth muscle contracts -> Arteriole circumference narrows reducing its radius -> Resistance increases and decreases blood flow through the vessel

VASODILATION = Smooth muscle relaxes -> Enlargement of the vessel’s circumference and radius -> Decreased resistance and increased blood flow through the vessel

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7
Q

What is the extent of contraction of arteriolar smooth muscle determined by?

A

The concentration of cystolic Ca2+

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8
Q

What does “Arteriolar smooth muscle normally exhibits vascular tone” mean?

A

There is a partial constriction that establishes a baseline level of arteriolar resistance

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9
Q

What is Vascular tone maintained by?

A
  • Smooth muscles with surface-membrane VOLTAGE-GATED CA2+ CHANNELS that are open even at RESTING POTENTIAL -> Triggers partial contraction
  • Continuous release of NOREPINEPHRINE by sympathetic fibers supplying most arterioles, further enhancing vascular tone
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10
Q

What does Vascular tone allow?

A

For the modulation of contractile activity, enabling vasoconstriction and vasodilation

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11
Q

What differentiates vascular smooth muscle from skeletal and cardiac muscle?

A

Vascular smooth muscle can undergo graded changes in force without action potentials

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12
Q

What are the categories that factors that influence arteriolar vasoconstriction or vasodilation fall into?

A
  • LOCAL (INTRINSIC) CONTROLS = play a role in determining the distribution of cardiac output
  • EXTRINSIC CONTROLS = involved in blood pressure regulation
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13
Q

What are Local (Intrinsic) controls?

A

Changes within an organ that affect blood flow through the organ by influencing the caliber and resistance of the organ’s arterioles, primarily through smooth muscle adjustments

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14
Q

What is the difference between Chemical and Physical influences on arteriolar radius?

A
  • CHEMICAL INFLUENCES = local metabolic changes and the release of histamine
  • PHYSICAL INFLUENCES = extent of vessel stretching, shear stress and local application of heat or cold
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15
Q

What can the distribution of Cardiac Output delivered to each organ depend on?

A
  • Demand for blood at a given time
  • Number and caliber of arterioles supplying each organ
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16
Q

The driving pressure gradient for blood flow is the same for all organs since blood is delivered at the same mean arterial pressure (TRUE/FALSE)

A

TRUE

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17
Q

How are variations in blood flow to different organs primarily influenced?

A
  • Differences in vascularisation
  • Resistance offered by arterioles supplying each organ
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18
Q

Why does the brain’s blood supply remain relatively constant regardless of the activity being performed?

A

The brain requires a consistent blood flow

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19
Q

Local metabolic changes can dynamically adjust blood flow without involving nerves or hormones (TRUE/FALSE)

A

TRUE

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20
Q

Describe Active Hyperaemia

A

As actively metabolising cells utilise more O2 for ATP production, the local O2 concentration decreases -> Local chemical changes trigger relaxation of the arteriolar smooth muscle, leading to LOCAL ARTERIOLAR DILATION -> LOCAL ARTERIOLAR VASODILATION increases blood flow to the specific area (ACTIVE HYPEREMIA) -> Active hyperaemia ensures that actively metabolising tissues receive increased blood flow to supply oxygen, nutrients and remove metabolic wastes

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21
Q

Describe how local chemical changes act to influence arteriolar radius

A
  • DECREASED O2 = triggers arteriolar relaxation
  • INCREASED O2 = by product of increased oxidative phosphorylation -> arteriolar relaxation
  • INCREASED ACID = increased carbonic and lactic acid -> arteriolar relaxation
  • INCREASED K+ = rapid action potentials that surpass the capacity of the Na+K+ pump to restore resting concentration gradients cause an elevation in interstitial fluid potassium levels in more active tissues
  • INCREASED OSMOLARITY = elevated cellular metabolism -> increase in osmolarity -> arteriolar relaxation
  • ADENOSINE RELEASE = arteriolar relaxation in cardiac muscle
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22
Q

What do Endothelial cells function in?

A

Regulating arteriolar caliber

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23
Q

What is Nitric Oxide (NO)?

A

A vasoactive paracrine that promotes arteriolar vasodilation by increasing intracellular cyclic GMP levels and reducing myosin phosphorylation leading to smooth muscle relaxation

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24
Q

What is the function of Nitric Oxide (NO)?

A
  • Regulates mean arterial pressure
  • Released in response to local metabolic changes promoting vasodilation
25
Q

What is Endothelin?

A

A potent vasoconstrictor and chemicals that trigger long-term vascular changes in response to chronic alterations in blood flow

26
Q

What is Vascular Endothelial Growth Factor (VEGF)?

A

A paracrine that stimulates ANGIOGENESIS (the growth of new blood vessels in response to chronic changes in blood flow)

27
Q

What is the difference between Active hyperaemia and Reactive hyperaemia?

A

ACTIVE HYPERAEMIA = occurs in response to changes in local chemical composition resulting from changes in local metabolic activity

REACTIVE HYPERAEMIA = occurs when the blood supply to a region is completely occluded while metabolic activity remains constant

28
Q

Describe Reactive Hyperaemia

A

Tissue continues to consume oxygen but does not receive fresh supplies due to OCCLUSION -> Decrease in oxygen levels and accumulation of CO2, acid and other metabolites -> Local chemical changes in blood-deprived tissue cause ARTERIOLAR DILATION in the area but occlusion PREVENTS BLOOD FLOW through dilated vessels -> After occlusion is removed, there is a transient increase in blood flow to previously deprived tissue due to widely dilated arterioles (REACTIVE HYPERAEMIA)

29
Q

What is the major difference between Active hyperaemia and Reactive hyperaemia?

A

ACTIVE HYPERAEMIA = increased local metabolic activity & blood flow to an organ is proportional to its metabolic activity

REACTIVE HYPERAEMIA = local blockage of blood supply & an increase in blood flow to an organ occurs after a period of occlusion of flow
[the longer the period of occlusion -> the greater the increase in blood flow is above preocclusion levels]

30
Q

What is Reactive hyperaemia beneficial for?

A

Restoring the local chemical composition to normal

31
Q

What does local histamine release do?

A

Pathologically dilates arterioles -> Histamine promotes relaxation of arteriolar smooth muscle -> Vasodilation in the injured area -> Increases blood flow -> Redness and swelling in inflammatory responses

32
Q

What are the properties of Histamine?

A
  • NOT released in response to local metabolic changes
  • NOT derived from endothelial cells
  • Synthesised and stores in certain cells in ORGANS and CIRCULATING WHITE BLOOD CELLS
33
Q

When is Histamine released?

A

During organ injury or allergic reactions

[Histamine is released and acts as a paracrine in the damaged region]

34
Q

How do Arteriolar smooth muscle respond to passive stretch?

A

Increasing its tone through vasoconstriction

MECHANISM: Increased stretching of the arterioles leads to the opening of MECHANICALLY GATED CATION CHANNELS -> DEPOLARISATION and OPENING of voltage-gated Ca2+ channels -> Ca2+ entry promotes increased smooth muscle contraction -> Vasoconstriction

35
Q

What does a reduction in arteriolar stretching cause?

A

Decrease in myogenic vessel tone through vasodilation

36
Q

What are the properties of the passive stretch of arterioles?

A
  • Varies with the volume of blood delivered
  • Influenced by mean arterial pressure (MAP)
37
Q

What happens when MAP is high and when it is decreased?

A

SUSTAINED ELEVATIONS IN MAP = Triggers vasoconstriction through the myogenic response, reducing tissue blood flow despite the elevated blood pressure

DECREASE IN MAP = Arterioles myogenically relax to compensate for reduced stretch, restoring tissue blood flow

38
Q

What is Autoregulation and what is its function?

A

Autoregulation = The combination of myogenic and chemical mechanisms that maintain relatively constant tissue blood flow despite changes in MAP

Autoregulatory responses bring tissue flow back to normal within a few minutes after the initial change in driving pressure

39
Q

Which organs are better at autoregulation?

A

Brain and kidneys compared to Skeletal muscle

40
Q

What is Shear?

A

A consequence of the fact that adjacent layers of blood travel at different velocities within a blood vessel

41
Q

Describe the mechanism of Shear

A

Velocity of blood is ZERO at the wall and HIGHEST at the centre of the vessel -> Shear is highest at the wall where the DIFFERENCE in blood velocity of adjacent layers is GREATEST -> Shear is lowest at the centre of the vessel where blood velocity is CONSTANT

42
Q

What are the effects of heat and cold application?

A

HEAT APPLICATION = promotes localised arteriolar vasodilation -> increasing blood flow to the area

COLD COMPRESS = induces vasoconstriction -> counteracts histamine-induced vasodilation and reduces swelling

43
Q

What is extrinsic control of arteriolar radius essential in?

A

Regulating blood pressure

44
Q

What does increased and decreased sympathetic activity cause?

A

INCREASED SYMPATHETIC ACTIVITY = generalised arteriolar vasoconstriction

DECREASED SYMPATHETIC ACTIVITY = generalised arteriolar vasodilation

45
Q

Describe the effect of Norepinephrine on the body

A

Norepinephrine related from SYMPATHETIC NERVE ENDINGS bind to a1-adrenergic receptors n arteriolar smooth muscle -> Vasoconstriction -> CEREBRAL arterioles do not have a1 receptors -> Not constricted by neural influences to maintain constant blood flow and meet the brain’s metabolic needs

46
Q

What is the function of Sympathetic activity?

A
  • Contributes to maintaining mean arterial pressure (MAP)
  • Ensures sufficient blood flow to the brain at the expense of other organs
47
Q

How is vasodilation usually achieved?

A
  • Parasympathetic innervation in the PENIS and CLITORIS
  • In other areas, by reducing sympathetic vasoconstrictor activity
48
Q

What region of the brain is responsible for adjusting sympathetic output to the arterioles and serves as the integrating centre for blood pressure regulation?

A

The cardiovascular control centre in the medulla of the brain stem

49
Q

How does the hypothalamus influence blood distribution?

A

By controlling blood flow to the skin as part of its temperature-regulating function

50
Q

Which hormones influence arteriolar radius and blood pressure regulation?

A
  • Epinephrine
  • Norepinephrine
  • Vasopressin
  • Angiotensin II
51
Q

How does Epinephrine work?

A

Epinephrine activates b2 receptors in skeletal muscles and the heart -> Vasodilation in tissues with these receptors

52
Q

How do Vasopressin and Angiotensin II work?

A

Vasopressin plays a role in maintaining WATER BALANCE by regulating KIDNEY FUNCTION and Angiotensin II regulates SALT BALANCE -> Potent vasoconstrictors that maintain blood pressure during haemorrhage by restoring BLOOD VOLUME and counteracting the LOSS OF BLOOD -> Influence fluid balance affecting blood volume and blood pressure regulation

53
Q

What are the properties of Renin-angiotensin-aldosterone system?

A
  • A slow, hormonal mechanism
  • Used in long-term blood pressure regulation by adjustment of blood volume
  • RENIN is an enzyme
  • ANGIOTENSIN I is inactive and ANGIOTENSIN II is physiologically active
54
Q

Describe the steps in the Renin-angiotensin-aldosterone system

A

1) A decrease in RENAL PERFUSION PRESSURE causes the JUXTAGLOMERULAR CELLS of the afferent arteriole to secrete RENIN which catalyses the conversion of ANGIOTENSINOGEN to ANGIOTENSIN I in plasma
2) ANGIOTENSIN-CONVERTING ENZYME (ACE) catalyses the conversion of angiotensin I to ANGIOTENSIN II in the lungs
3) Angiotensin II has four effects
- Stimulates synthesis and secretion of ALDOSTERONE by the ADRENAL CORTEX (increases Na+ reabsorption -> increases ECF volume, blood volume and arterial pressure)
- Increases Na+-H+ exchange (increases Na+ reabsorption)
- Increases thirst -> Increased water intake
- Causes vasoconstriction of arterioles

55
Q

How do ACE inhibitors and Angiotensin receptor antagonists work?

A

ACE INHIBITORS = block the conversion of angiotensin I to angiotensin II -> decreases blood pressure

ANGIOTENSIN RECEPTOR ANTAGONISTS = block the action of angiotensin II at its receptor and decrease blood pressure

56
Q

Why is the action of Aldosterone slow?

A

It requires new protein synthesis

57
Q

What is The Renin-Agiotensin-Aldosterone System (RAAS)?

A

A complex hormonal system involved in regulating blood pressure, fluid balance and electrolyte homeostasis in the body

58
Q

What is Angiotensin II?

A

A potent vasoconstrictor causing the narrowing of blood vessels which increases peripheral resistance and elevates blood pressure

[It also stimulates the release of ALDOSTERONE from the adrenal glands]

PHYSIOLOGY II (15 decks)

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