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Physiology Exam 2 > L12: Control of Blood Flow > Flashcards

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
vasopressin
vasoconstrictor also called ADH very powerful vasoconstrictor major function is to control body fluid volume
26
humoral circulation control: vasodilators
1. bradykinins | 2. histamine
27
bradykinins
cause both vasodilation and increased capillary permeability
28
histamines
powerful vasodilator derived from mast cells and basophils
29
sympathetic system: circulation
1. innervates all vessels except capillaries | 2. stimulation primarily results in vasoconstriction
30
what secretes epinephrine and norepinephrine
adrenal medulla
31
list the vasomotor centers in the brain
1. vasoconstriction area 2. vasodilation area 3. sensory area 4. other
32
vasoconstriction area in brain
1. upper medulla | 2. transmits continuous signals to BVs
33
vasomotor tone
= partial state of contraction of blood vessels
34
vasoconstrictor area continuous firing
results in sympathetic vasoconstrictor tone
35
vasodilator area of brain
lower medulla | inhibits vasoconstrictor area activity
36
sensory area of brain vasomotion
in medulla and both sides of brain receives signals from vagus and glossopharyngeal nerves
37
other areas of vasomotor control in brain
1. brain stem (reticular substance) 2. hypothalamus 3. cerebral cortex
38
baroreceptors in carotids and aorta
inhibit vasoconstrictor center and stimulate vasodilator center
39
carotid bodies
present in aorta and carotids - chemosensitive cells - more important for respiratory control
40
neural rapid control of atrial pressure
- cause simultaneous changes - rapid response w/in seconds - ex. increased blood pressure during exercise, flight or fight responses
41
what changes can the brain induce to control atrial pressure
simultaneous changes - constriction of most systemic arteries - constriction of veins - increased heart rate
42
what causes constriction vs. dilation of vessels?
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
baroreceptors
- pressure receptors stimulated by low arterial pressure - located in aorta and carotids - vagus nerves - glossopharyngeal nerves
44
baroreceptors pressure limits
aorta - press > 80-200 carotid - press > 60-180
45
other locations of baroreceptors
reticular substance hypothalamus cerebral cortex
46
signals from baroreceptors
- 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
chemoreceptors
- 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
reflex dilation of kidney afferent arterioles
increases kidney fluid loss decreases blood volume decreases pressure
49
atrial reflexes responding to increase in atrial stretch
- dilation of kidneys - increase HR - signals to hypothalamus (decrease ADH conc.) - atrial natriuretic peptide ANP - decrease Na+ absorption
50
ANP
sends signals to kidneys increase GFR decrease Na+ absorption to increase fluid loss an atrial reflex in response to stretching
51
what is the result of decreasing Na+ absorption
cells don't absorb Na so it is lost to urine
52
arterial pressure =
CO x total peripheral resistance
53
arterial pressure rises when
total peripheral resistance is acutely increased normal functioning kidneys return arterial pressure back to normal w/in few days
54
normal kidney function is capable of maintaining normal arterial pressure even as ….
CO ranges from 40 - 160% of normal output
55
primary or essential hypertension
- unknown origin - 90-95% of hypertension - major factors: weight gain and sedentary lifestyle
56
secondary hypertension
- hypertension second to some other cause | - examples: tumors, renal artery constriction, preeclampsia, neural, genetic
57
contributing factors to hypertension
``` -genetics gene disorders renin-angiotensin sys. stress obesity smoking inactivity high salt intake ``` overall concept: multifaceted, caused by a variety of different factors
58
factors resulting in decreased peripheral resistance = decreased BP
- increased production of NO, release of prostacyclin and kinins and ANP - decreased neural factors
59
factors resulting in decreased cardiac output leading to decreased BP
-decreased blood vol., HR, contractility of heart
60
vasoconstrictors
angiotensin II catecholamines endothelin
61
vasodilators
kinins prostaglandins NO
62
lethal effects of chronic hypertension
- early heart failure and coronary artery disease - cerebral infarction - kidney failure
63
atherosclerosis
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
non-modifiable risk factors of atherosclerosis
- age - gender - genetics
65
define hyperhomocystinemia
inborn error of metabolism
66
pathogenesis of atherosclerosis
- endothelial injury or dysfunction of any kind - accumulation of lipoproteins - monocyte adhesion to endothelium
67
atheroma morphology
- consists of a cap of smooth muscle cells, macrophages, foam cells, and other extracell components - this occurs within the vessels
68
early stage of atherosclerosis
- early lesions are fatty streaks - plaques forming white/yellow - plaques can be calcified, rupture or erode
69
common sites of atherosclerosis
- lower aorta - coronary art. - carotid art.
70
convert macrophages
foam cells
71
long term control of arterial pressure
- nervous and hormone control | - kidneys
72
relate urinary output and arterial pressure
positive correlation
73
pressure diuresis
increase urine output
74
pressure natriuresis
increase sodium output
75
near infinite feedback gain principle
return of arterial pressure back to equilibrium point
76
primary determinants of long-term arterial pressure level
- degree of pressure shift of the renal output curve for water/salt - level of water/salt intake
77
acute increases in blood pressure cause 2-3x increase in _____ ____ output. which is independent of ______ .
urinary Na output | independent of sympathetic system of hormones
78
over a long period, water and salt ____ must equal _____ .
output = input
79
increased intake of salt and water increases?
arterial pressure via kidney function
80
chronic increases intake of salt and water: effects on renal curve aka arterial pressure
curve becomes near vertical so arterial pressure is not significantly elevated since it is a chronic condition
81
acute vs chronic effects on renal curve to arterial pressure
acute = significant increase in arterial pressure chronic very little increase in arterial pressure (means chronic or acute high intake of salt and water)
82
define chronic hypertension
one's mean arterial pressure is greater than the upper range of the accepted normal measure aka chronic high blood pressure
83
normal vs hypertensive vs. severe hypertensive BP
90 -- 110/70 110 -- 135/90 150 -- 250/130 (90 = mean pressure)
84
lethal effects of chronic hypertension
1. early heart failure 2. coronary heart disease 3. MI 4. cerebral infarct 5. kidney failure
85
destruction of areas of kidneys
= kidney failure = uremia =death
86
renin-angiotensin system
something causes a decrease in blood pressure this system works to increase pressure
87
steps of renin-angiotensin system
1. decreased arterial press. 2. effects renin sys. 3. kidney releases renin 5. angiotensinogen converted to angiotensin I 6. angiotensin I converted to angiotensin II 7. II acts 8. bp increased
88
effects of angiotensin II
1. on kidneys to retain salt and water 2. acts on adrenal gland to release aldosterone 3. vasocontriction 4. inactivate angiotensinase
89
what does renin do?
the liver produces angiotensinogen renin converts this to angiotensin I
90
why must angiotensin I be converted?
I is inactive forms enzyme ACE from lungs and endothelium tissues convert angiotensin I to II which active form
91
renin-angiotensin system for increased salt intake
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
ACE
angiotensin converting enzyme

Physiology Exam 2 (9 decks)

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