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PHYSIOLOGY Exam 3 (Lauren) > Regional Circulations > Flashcards

Regional Circulations Flashcards

1
Q

What does hyperemia mean?

A

Increased blood flow

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2
Q

What are extrinsic mechanisms that regulate blood flow?

A

Hormonal/neural control

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3
Q

What is “the contractile state of a resistance vessel?”

A

Tone

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4
Q

What is basal tone?

A

The state of partial contraction independent of metabolic and neural mechanisms

A result of the properties of the vessel vascular smooth muscle

(If you removed the vessel from all other inputs and put it in a chamber, how much tone you would have)

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5
Q

How does the resting tone of vessels differ from the basal tone?

A

The resting tone of vessels is higher than what their basal tone would be due to tonic sympathetic nerve activity

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6
Q

What is active vasoconstriction?

A

A decrease in vessel diameter due to sympathetic stimulation or constrictor hormones

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7
Q

What is active vasodilation?

A

Increase in vessel diameter due to dilator nerves, hormones, or local factoss

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8
Q

What is passive vasoconstriction?

A

A return towards resting state from a dilated state due to the removal of active dilator influences

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9
Q

What is passive vasodilation?

A

A return towards resting state from a constricted state due to the removal of active constrictor influences

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10
Q

Is autoregulation dependent on neural input?

A

No it is entirely independent of neural input

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11
Q

What is autoregulation/

A

A tissue doing what it has to do to maintain a steady-state pressure despite fluctuation in blood pressure

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12
Q

What are the 2 theories that can explain how tissues auto regulate their blood flow to a steady state despite fluctuations in blood pressure?

A

Metabolic theory

Myogenic theory

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13
Q

How does the metabolic theory explain how tissues autoregulate their blood flow?

A

As perfusion pressure increases, vasodilator metabolites are washed out of the surrounding fluid causing passive vasoconstriction and an increase in resistance (and conversely, metabolites accumulate when pressure falls)

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14
Q

How does the myogenic theory explain how tissues autoregulate their blood flow?

A

Increases in pressure causes the walls to stretch, which opens up calcium channels, which causes vascular smooth muscle to contract, and increasing resistance

(And conversely, vasodilation occurs when pressure falls and wall tension decreases)

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15
Q

What are some examples of metabolic vasodilators?

A

K+

CO2

Local hypoxia (sort of)

Lactic acid

H+

Phosphate ions

Prostaglandins

Adenosine

Adenine nucleotides

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16
Q

How does active tissue tell the arterioles that it needs more blood and they need to dilate?

A

Active tissue will release metabolic vasodilators

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17
Q

What is active hyperemia?

A

Blood flow is adjusted to meet the metabolic demands of the tissue

-accomplished via an increased production of vasodilator metabolites

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18
Q

What is reactive hyperemia?

A

The increase in blood flow to a tissue that occurs in response to transient ischemia

Caused by the local buildup of vasodilator metabolites during the ischemic phase

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19
Q

Duration and magnitude of reactive hyperemia are proportional to the ______

A

Length of time of the ischemia

20
Q

Does reactive hyperemia happen all the time everyday

A

Yes for example when you bench press at the gym and occlude blood flow momentarily, that qualifies as transient ischemia, and metabolic vasodilators will accumulate

21
Q

What happens if norepinephrine binds to an a-1 adrenergic receptor on vascular smooth muscle of resistance vessels and veins?

A

vasoconstriction

22
Q

What happens if you withdraw sympathetic activity?

A

Passive vasodilation

23
Q

Which receptor does epinephrine bind to to cause contraction?

A

a-1 receptors

24
Q

Which receptor does epinephrine bind to to cause relaxation, and where are they mainly located?

A

B2-adrenergic receptors mainly located in skeletal muscle

25
Q

What is the effect of epinephrine release?

A

Most tissues —> vasoconstriction

Skeletal muscle —> vasodilation (due to having more B2 receptors)

26
Q

What does angiotensin II do?

A

Potent vasoconstriction that acts directly on vascular smooth muscle of resistance vessels

27
Q

What effect does angiotensin II have on the adrenal cortex?

A

It controls the release of aldosterone

Enhances sodium reabsorotion in kidneys which also enhances reabsorption of water

28
Q

Angiotensin II is synthesized when blood pressure is (high/low)

A

Low

29
Q

What receptors does angiotesnsin II bind to on vascular smooth muscle of resistance vessels?

A

AT1 receptors

30
Q

Is angiotensin a pressor?

A

Yes it is a very powerful pressor

31
Q

What is vasopressin?

A

A peptide that is released from the posterior pituitary in response to low blood pressure (or rising plasma osmolality)

It is a potent vasoconstriction that acts directly on vascular smooth muslce of resistance vessels

32
Q

What receptor does vasopressin bind to on the vascular smooth muscle of resistance vessels?

A

V1 receptors

33
Q

what is another name for anti diuretic hormone

A

Vasopressin

34
Q

What effect does histamine have on vascular smooth muscle tone?

A

Dilates arterioles

Constricts venues

Makes capillaries leaky

(Causes angioedema)

35
Q

Why is it important to maintain vascular tone in skeletal muscle?

A

Because its 40-45% of your body weight and maintains a large amount of resistance vessels. If the tone fell, your BP would crash entirely

36
Q

What dominates the regulation of vascular tone of skeletal muscle at rest?

A

Neural control that is regulated by a-1 adrenergic receptors and norepinephrine***!!!!

It is part of the TONIC sympathetic nervous system

(Remember that anytime you stimulate a-1 receptors, the result is vasoconstriction)

Also we want to maintain a certain amount of vascular tone in skeletal muscle at all times

37
Q

What will the result be of an a-1 adrenergic receptor being stimulated

A

Vasoconstriction, always

38
Q

What are the main metabolic vasodilators of skeletal muscles?

A

Lactate

K+

Adenosine

39
Q

When are vasodilator metabolites dominant in skeletal muscle?

A

During exercise

Although SNS tonic activity may also be present, but it is overwhelmed by the effect of the vasodilator metabolites

40
Q

What are the major metabolic vasodilators in the coronary circulation

A

Adenosine

Nitric Oxide (NO)

41
Q

Which has a larger role in the control of blood flow to the coronary circulation: local metabolites or sympathetic innervation?

A

Local metabolites, by far

42
Q

Why doesnt increased SNS activity cause vasoconstriction of the coronary arteries?

A

It is completely overwhelmed by the effect of the local metabolites

(Even though it is activation of a-1 receptors, which always causes vasoconstriction)

43
Q

When do the coronary vessels receive most of their blood flow?

A

Diastole

44
Q

During systole, the coronary vessels are temporarily occluded. Does this result in transient ischemia, and therefore reactive hyperemia?

A

yes it does. The occlusion allows for the buildup of vasodilator metabolites so the coronary vessels will dilate.

45
Q

Why do you see a peak in coronary artery blood flow right at the end of systole?

A

Due to the buildup of metabolic vasodilators when the flow was briefly occluded during diastole (reactive hyperemia)

46
Q

What are the 2 effects of sympathetic stimulation on the coronary arteries and arterioles?

A
  1. Norepinephrine —a1 receptor—constriction
    (**overcome by local metabolites)
  2. Epinephrine —B2–vasodilation
47
Q

What are the 2 effects of SNS stimulation on the heart muscle?

A
  1. B1 receptors —> increased HR, increased contractility

2. Local metabolism —> vasodilators —> increased blood flow

PHYSIOLOGY Exam 3 (Lauren) (10 decks)

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