Lesson 24: Topic 20 - Regulation of Blood Flow Flashcards

1
Q

the stimuli that causes vasodilation or vasoconstriction originates where?

A

in the specific tissue or organ which will then be a local regulatory mechanism
OR
can originate ‘centrally’ which will then be a systemic regulatory mechanism

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2
Q

what is the purpose of having a local regulation of blood flow?

A

it is designed to ensure that a specific organ receives the blood flow it wants (not to regulate MAP)

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3
Q

when a stimuli to cause vasodilation or constriction originates centrally, what is the main purpose?

A

to regulate MAP

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4
Q

what does “intrinsic” regulatory mean in regards to local control of blood flow?

A
  • signals within an organ are responsible for controlling blood flow to that organ
  • not dependent on nerves or circulating hormones
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5
Q

what are the “intrinsic” regulatory mechanisms of local control of blood flow?

A
  1. active hyperemia / reactive hyperemia
  2. flow auto-regulation
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6
Q

what is active hyperemia / reactive hyperemia driven by?

A

a metabolite-dependent mechanism

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7
Q

what does hyperemia refer to?

A

an increase in blood flow

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8
Q

what is flow auto-regulation

A

somehow we are maintaining blood flow to a given organ

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9
Q

true or false: as tissue metabolic activity increase, so does blood flow.

A

true

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10
Q

active hyperemia occurs where?

A

in tissues with high but variable metabolic need like the skeletal muscle and the WITHIN brain (the blood within the brain already is being diverted to areas within the brain with high metabolic activity)

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11
Q

what type of feedback loop is active hyperemia?

A

negative feedback loop

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12
Q

what is the negative feedback loop of active hyperemia?

A

increased metabolic activity –> decreased O2 concentration and increases metabolites concentration like K+ and ATP –> nitric oxide production and smooth muscle relaxation –> vasodilation of arterioles –> increased blood flow –> reduces hyperemic response because the increased blood flow increases O2 concentration to then decrease metabolites and start back at step 2 (but nothing else happens)

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13
Q

why is active hyperemia a negative feedback loop?

A

because once blood flow increases, it then goes to increase O2 concentration to stop the feedback loop and reduce the active hyperemia response and cause vasoconstriction

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14
Q

what type of feedback loop is reactive hyperemia?

A

negative feedback loop

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15
Q

what is an example of when we will need to use reactive hyperemia?

A

ischemia

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16
Q

what starts / activates reactive hyperemia?

A

lack of blood flow
- often caused by a temporary compression of blood vessels

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17
Q

whats the difference between active and reactive hyperemia?

A

active hyperemia is activated by metabolic activity and reactive hyperemia is activated by lack of blood flow
- the rest of the process is the same otherwise, even the negative feedback loop

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18
Q

where does reactive hyperemia happen?

A

in skeletal muscle. if we have a very big contraction during exercise, that will stop blood blow and reduce blood flow and increase metabolites so we will relax our skeletal muscles, blood blow perfusion increases in skeletal muscle

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19
Q

what does occlude blood flow mean?

A

stop blood flow

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20
Q

when does reactive hyperemia happen?

A

during heart or skeletal muscle contraction
- also because of a blood pressure cuff

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21
Q

ventricular contraction is the accumulation of?

A

metabolites

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22
Q

during diastole, there is a period of flow recovery during ventricular relaxation, which type of local intrinsic control of blood flow is this because of?

A

reactive hyperemia

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23
Q

where does flow auto-regulation occur?

A

in the kidney, brain

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24
Q

what is the definition of flow auto-regulation?

A

blood flow to an organ is kept steady despite changes in BP or pressure gradients (delta P)

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25
Q

when can flow auto-regulation not occur in blood flow?

A

not at very low pressure or very high pressures
- because you cannot vasoconstrict strongly enough or vasodilate more than physiologically possible

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26
Q

vasoconstriction is maintained by?

A

smooth muscle

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27
Q

why is flow auto-regulation important in the kidneys?

A

because you want to make sure that the kidneys are filtering the blood and if you have too high of pressures, you do not want to exceed the ability of the kidneys to filter the blood and too high of blood flow to damage the kidneys

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28
Q

what is flow auto-regulation due to?

A

the myogenic response

29
Q

what is a myogenic response?

A

refers to a reflux response of the arterioles to change blood pressure

30
Q

what does myo mean?

31
Q

true or false: flow auto-regulation is a muscle dependent response.

32
Q

in flow auto-regulation, increased arterial blood pressure leads to?

A

passive distension of arteriole wall
- AKA leading to a passive stretch of the arteriole wall

33
Q

a passive stretch of the arteriole wall does what to the arteriole? (hint: diameter)

A

increases the arteriole diameter (makes sense because the wall is being stretched)

34
Q

when we have increased arteriole diameter, what happens?

A

vasodilation which leads to increased blood flow

35
Q

what happens to the smooth muscle cells when the arteriole wall is being stretched?

A

smooth muscle cells also stretch (they are literally apart of the arteriole silly)

36
Q

an increase in the stretch of the smooth muscle cells triggers what?

A

an increase in the cytosolic calcium inside the smooth muscle

37
Q

an increase in cytosolic calcium concentration will increase?

A

force generation of that muscle (increases contraction which will cause vasoconstriction in order to reduce blood flow)

38
Q

what type of feedback loop is flow auto-regulation?

A

negative feedback loop

39
Q

why is flow auto-regulation a negative feedback loop?

A

because we decrease blood flow which will then cause the blood vessel walls to relax and allowing blood flow to increase

40
Q

local regulatory mechanisms of blood flow is always which feedback loop?

41
Q

if our smooth muscle is contracting more, does this cause the arteriole to constrict or dilate?

42
Q

low O2 and high CO2 causes vaso?

A

vasodilation (we want more blood flow for more oxygen)

43
Q

high NO generation causes vaso?

A

vasodilation

44
Q

increased endothelin causes?

A

vasoconstriction as well to reduce muscle blood flow at the level of the arteriole

45
Q

true or false: vasodilation is caused by decreased stretch reflex activity.

46
Q

what is systemic control of blood flow controlled by?

A
  1. neural
  2. hormonal
47
Q

the neural systemic control of blood flow is regulated by?

A

the sympathetic nervous system

48
Q

what is the main purpose of the systemic control of blood flow?

A

the regulate MAP

49
Q

true or false: there is no influence of the parasympathetic nervous system on the blood vessels or blood flow regulation.

50
Q

what is the baseline state (regular state) for the sympathetic nerves?

A
  • sympathetic nerve is activated by CNS (response to stress or exercise)
  • cause sympathetic neuron to fire
  • produce repeated action potentials
  • going to stimulate the sympathetic neuron
  • increase sympathetic neuron activity
  • going to produce norepinephrine
  • norepinephrine attaches to alpha-adrenergic receptors that are located throughout the whole entire body but mostly on the smooth muscle
  • causes vasoconstriction
51
Q

what happens to SNS activity during exercise?

A

increased SNS activity

52
Q

how does exercise cause more vasoconstriction?

A

increased SNS activity, more norepinephrine to attach to a-adrenergic receptor on smooth muscle to cause vasoconstriction

53
Q

after exercise, SNS activity decreases. how does this cause vasodilation?

A

firing of APs and sympathetic neuron are low so that decreases the production or norepinephrine which leads to vasodilation

54
Q

increased vasoCONSTRICTION means what from MAP?

A

increases MAP

55
Q

constriction on the venous side of the vascular system is called?

A

vENoconstriction

56
Q

smooth muscle cells of arterioles and venules have alpha adrenergic receptors which cause?

A

vaso/veno-constriction

57
Q

arterioles in skeletal muscle have beta adrenergic receptors which induce?

A

vasodilation

58
Q

what does beta adrenergic receptors do?

A

counter the effects of alpha adrenergic receptors

59
Q

there is a greater binding affinity for norepinephrin or epinephrine on alpha adrenergic receptors?

A

norepinephrine

60
Q

there is a great binding affinity for norepinephrine or epinephrine on beta adrenergic receptors?

A

epinephrine

61
Q

epinephrine is produced by?

A

the adrenal medulla gland

62
Q

epinephrine produced by the adrenal medulla gland is released into?

63
Q

when epinephrine binds to the beta adrenergic receptors, it causes?

A

vasodilation

64
Q

in the arterioles, are there more alpha or beta adrenergic receptors?

A

more alpha adrenergic receptors in the arterioles

65
Q

true or false: by activating beta adrenergic receptors, there is less vasoconstriction than if only alpha adrenergic receptors were active

A

true
- b-adrenergic counters the affects of alpha adrenergic receptors

66
Q

epinephrine causes vasodilation via?

A

beta adrenergic receptors

67
Q

true or false: usually both norepinephrine and epinephrine are present

68
Q

true or false: both norepinephrine and epinephrine can bind to the alpha adrenergic receptor