L12: Control of Blood Flow Flashcards

1
Q

acute control of local blood flow

A
  1. rapid changes in local vessel diameters
  2. occurs in seconds or minutes
  3. basic theories = vasodilator and oxygen lack theories
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2
Q

long-term control of local blood flow

A
  1. increase in sizes/number of vessels

2. occurs over a period of days to months

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3
Q

describe the acute control vasodilator theory

A

increased metabolism
= decreased oxygen
=formation of vasodilators

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4
Q

list examples of vasodilators

A
  1. adenosine
  2. co2
  3. adenosine Pi compounds
  4. histamine
  5. K+ ions
  6. H+ ions
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5
Q

describe the acute control oxygen lack theory

A

increased metabolism
= decreased oxygen
= BV relaxation
= vasodialtion

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6
Q

relate vasomotion to tissue requirements and what is the assumption

A

of precapillary sphincters open is proportional to nutritional requirements of tissues

assumes smooth muscle requires oxygen to remain contracted

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7
Q

describe reactive hyperemia

A

when tissue blood flow is blocked for some reason

  • after unblocked
  • tissue flow increases 4-7x normal because this tissue went w/o nutrients
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8
Q

describe active hyperemia

A

when a tissue becomes active, such as exercise

the rate of blood flow to that tissue will increase

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9
Q

increase in metabolism vs. tissue blood flow

A

increased metabolism = increased flow

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10
Q

effect of decreased arterial oxygenation saturation on blood flow

A

when o2 levels decrease = blood flow increases

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11
Q

autoregulation

A
  • occurs in any tissue
  • rapid increase in arterial pressure = increased flow

within minutes blood flow can return to normal even in the presence of increased pressure

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12
Q

theories to explain autoregulation

A
  1. metabolic theory

2. myogenic theory

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13
Q

describe metabolic theory of autoregulation

A

increased blood flow
=too much o2 to tissues
= washes out vasodilators
= vasodilation to reduce flow when tissues are satisfied

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14
Q

describe myogenic theory of autoregulation

A

increased blood flow
= stretching of vessels
= reactive vasculature constriction
= reduced flow in response to stretching of vessels

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15
Q

special acute blood flow control mechanisms exist in the: ?

A

kidneys
brain
skin

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16
Q

kidney acute blood flow control

A

tubuloglomerular feedback – kidney tubules monitor flow and have special mechanisms to allow them to effect flow

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17
Q

brain acute blood flow control

A

increased co2 (also increased [H+])
=cerebral vessel dilation
=causes washing out of excess co2/H+

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18
Q

skin acute blood flow control

A

blood flow is linked to body temp.
symphathic nerves vis CNS

decrease flow in cold weather (3mL tissue)
increase in hot (7-8L entire body)

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19
Q

endothelium derived mechanism for blood flow control

A

healthy endothelial cells release NO
=which converts cGTP to cGMP
=cGMP activates protein kinases
=kinases are vasodilators

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20
Q

how does hypertension effect endothelium control of blood flow

A

inhibits the release of NO

-so endothelium cannot induce vasodilators

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21
Q

blood flowing thru arteries and arterioles causes ____ stress which leads to endothelium releasing ____ .

A

shear stress

release of NO

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22
Q

list vasoconstrictors of humoral control

A
  1. norepinephrine
  2. epinephrine
  3. angiotensin II
  4. vasopressin
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23
Q

what is ADH

A

anti-diuretic hormone

causes the retaining of fluids

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24
Q

angiotensin II

A

vasoconstriction

acts to increase total peripheral resistance

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25
Q

vasopressin

A

vasoconstrictor
also called ADH
very powerful vasoconstrictor
major function is to control body fluid volume

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26
Q

humoral circulation control: vasodilators

A
  1. bradykinins

2. histamine

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27
Q

bradykinins

A

cause both vasodilation and increased capillary permeability

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28
Q

histamines

A

powerful vasodilator derived from mast cells and basophils

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29
Q

sympathetic system: circulation

A
  1. innervates all vessels except capillaries

2. stimulation primarily results in vasoconstriction

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30
Q

what secretes epinephrine and norepinephrine

A

adrenal medulla

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31
Q

list the vasomotor centers in the brain

A
  1. vasoconstriction area
  2. vasodilation area
  3. sensory area
  4. other
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32
Q

vasoconstriction area in brain

A
  1. upper medulla

2. transmits continuous signals to BVs

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33
Q

vasomotor tone

A

= partial state of contraction of blood vessels

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34
Q

vasoconstrictor area continuous firing

A

results in sympathetic vasoconstrictor tone

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35
Q

vasodilator area of brain

A

lower medulla

inhibits vasoconstrictor area activity

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36
Q

sensory area of brain vasomotion

A

in medulla and both sides of brain

receives signals from vagus and glossopharyngeal nerves

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37
Q

other areas of vasomotor control in brain

A
  1. brain stem (reticular substance)
  2. hypothalamus
  3. cerebral cortex
38
Q

baroreceptors in carotids and aorta

A

inhibit vasoconstrictor center and stimulate vasodilator center

39
Q

carotid bodies

A

present in aorta and carotids

  • chemosensitive cells
  • more important for respiratory control
40
Q

neural rapid control of atrial pressure

A
  • cause simultaneous changes
  • rapid response w/in seconds
  • ex. increased blood pressure during exercise, flight or fight responses
41
Q

what changes can the brain induce to control atrial pressure

A

simultaneous changes

  • constriction of most systemic arteries
  • constriction of veins
  • increased heart rate
42
Q

what causes constriction vs. dilation of vessels?

A

constrictor center tells smooth muscle to contract to constrict vessels

but we can not send signals for dilation we just tell the constrictor center to ease up

43
Q

baroreceptors

A
  • pressure receptors stimulated by low arterial pressure
  • located in aorta and carotids
  • vagus nerves
  • glossopharyngeal nerves
44
Q

baroreceptors pressure limits

A

aorta - press > 80-200

carotid - press > 60-180

45
Q

other locations of baroreceptors

A

reticular substance
hypothalamus
cerebral cortex

46
Q

signals from baroreceptors

A
  • inhibit vasoconstrictor center
  • excite vasodilator center
  • signals increase or decrease arterial pressure depending on situation
  • primary function is to reduce variations in arterial pressure
47
Q

chemoreceptors

A
  • located in carotids and aorta
  • sensitive to lack of O2, CO2 excess, or H+ excess
  • signals pass thru herring’s nerves and vagus nerves
  • important role in respiratory control
48
Q

reflex dilation of kidney afferent arterioles

A

increases kidney fluid loss

decreases blood volume

decreases pressure

49
Q

atrial reflexes responding to increase in atrial stretch

A
  • dilation of kidneys
  • increase HR
  • signals to hypothalamus (decrease ADH conc.)
  • atrial natriuretic peptide ANP
  • decrease Na+ absorption
50
Q

ANP

A

sends signals to kidneys
increase GFR
decrease Na+ absorption

to increase fluid loss

an atrial reflex in response to stretching

51
Q

what is the result of decreasing Na+ absorption

A

cells don’t absorb Na so it is lost to urine

52
Q

arterial pressure =

A

CO x total peripheral resistance

53
Q

arterial pressure rises when

A

total peripheral resistance is acutely increased

normal functioning kidneys return arterial pressure back to normal w/in few days

54
Q

normal kidney function is capable of maintaining normal arterial pressure even as ….

A

CO ranges from 40 - 160% of normal output

55
Q

primary or essential hypertension

A
  • unknown origin
  • 90-95% of hypertension
  • major factors: weight gain and sedentary lifestyle
56
Q

secondary hypertension

A
  • hypertension second to some other cause

- examples: tumors, renal artery constriction, preeclampsia, neural, genetic

57
Q

contributing factors to hypertension

A
-genetics
gene disorders
renin-angiotensin sys.
stress
obesity
smoking
inactivity
high salt intake

overall concept: multifaceted, caused by a variety of different factors

58
Q

factors resulting in decreased peripheral resistance = decreased BP

A
  • increased production of NO, release of prostacyclin and kinins and ANP
  • decreased neural factors
59
Q

factors resulting in decreased cardiac output leading to decreased BP

A

-decreased blood vol., HR, contractility of heart

60
Q

vasoconstrictors

A

angiotensin II
catecholamines
endothelin

61
Q

vasodilators

A

kinins
prostaglandins
NO

62
Q

lethal effects of chronic hypertension

A
  • early heart failure and coronary artery disease
  • cerebral infarction
  • kidney failure
63
Q

atherosclerosis

A

a type of arteriosclerosis or hardening of the arteries

  • major characteristic is presence of lesions within the intima of the vessel wall
  • resulting in increased BP or even blockage
64
Q

non-modifiable risk factors of atherosclerosis

A
  • age
  • gender
  • genetics
65
Q

define hyperhomocystinemia

A

inborn error of metabolism

66
Q

pathogenesis of atherosclerosis

A
  • endothelial injury or dysfunction of any kind
  • accumulation of lipoproteins
  • monocyte adhesion to endothelium
67
Q

atheroma morphology

A
  • consists of a cap of smooth muscle cells, macrophages, foam cells, and other extracell components
  • this occurs within the vessels
68
Q

early stage of atherosclerosis

A
  • early lesions are fatty streaks
  • plaques forming white/yellow
  • plaques can be calcified, rupture or erode
69
Q

common sites of atherosclerosis

A
  • lower aorta
  • coronary art.
  • carotid art.
70
Q

convert macrophages

A

foam cells

71
Q

long term control of arterial pressure

A
  • nervous and hormone control

- kidneys

72
Q

relate urinary output and arterial pressure

A

positive correlation

73
Q

pressure diuresis

A

increase urine output

74
Q

pressure natriuresis

A

increase sodium output

75
Q

near infinite feedback gain principle

A

return of arterial pressure back to equilibrium point

76
Q

primary determinants of long-term arterial pressure level

A
  • degree of pressure shift of the renal output curve for water/salt
  • level of water/salt intake
77
Q

acute increases in blood pressure cause 2-3x increase in _____ ____ output. which is independent of ______ .

A

urinary Na output

independent of sympathetic system of hormones

78
Q

over a long period, water and salt ____ must equal _____ .

A

output = input

79
Q

increased intake of salt and water increases?

A

arterial pressure

via kidney function

80
Q

chronic increases intake of salt and water: effects on renal curve aka arterial pressure

A

curve becomes near vertical so arterial pressure is not significantly elevated since it is a chronic condition

81
Q

acute vs chronic effects on renal curve to arterial pressure

A

acute = significant increase in arterial pressure

chronic very little increase in arterial pressure

(means chronic or acute high intake of salt and water)

82
Q

define chronic hypertension

A

one’s mean arterial pressure is greater than the upper range of the accepted normal measure

aka chronic high blood pressure

83
Q

normal vs hypertensive vs. severe hypertensive BP

A

90 – 110/70

110 – 135/90

150 – 250/130

(90 = mean pressure)

84
Q

lethal effects of chronic hypertension

A
  1. early heart failure
  2. coronary heart disease
  3. MI
  4. cerebral infarct
  5. kidney failure
85
Q

destruction of areas of kidneys

A

= kidney failure
= uremia
=death

86
Q

renin-angiotensin system

A

something causes a decrease in blood pressure

this system works to increase pressure

87
Q

steps of renin-angiotensin system

A
  1. decreased arterial press.
  2. effects renin sys.
  3. kidney releases renin
  4. angiotensinogen converted to angiotensin I
  5. angiotensin I converted to angiotensin II
  6. II acts
  7. bp increased
88
Q

effects of angiotensin II

A
  1. on kidneys to retain salt and water
  2. acts on adrenal gland to release aldosterone
  3. vasocontriction
  4. inactivate angiotensinase
89
Q

what does renin do?

A

the liver produces angiotensinogen

renin converts this to angiotensin I

90
Q

why must angiotensin I be converted?

A

I is inactive forms

enzyme ACE from lungs and endothelium tissues
convert angiotensin I to II which active form

91
Q

renin-angiotensin system for increased salt intake

A
  1. increase Na intake
  2. increased Extracellular fluid vol.
  3. increased arterial press.
  4. decreased renin and angiotensin
  5. decreased renal retention
  6. return of extra fluid to normal
  7. arterial pressure return to normal
92
Q

ACE

A

angiotensin converting enzyme