L12: Control of Blood Flow Flashcards
acute control of local blood flow
- rapid changes in local vessel diameters
- occurs in seconds or minutes
- basic theories = vasodilator and oxygen lack theories
long-term control of local blood flow
- increase in sizes/number of vessels
2. occurs over a period of days to months
describe the acute control vasodilator theory
increased metabolism
= decreased oxygen
=formation of vasodilators
list examples of vasodilators
- adenosine
- co2
- adenosine Pi compounds
- histamine
- K+ ions
- H+ ions
describe the acute control oxygen lack theory
increased metabolism
= decreased oxygen
= BV relaxation
= vasodialtion
relate vasomotion to tissue requirements and what is the assumption
of precapillary sphincters open is proportional to nutritional requirements of tissues
assumes smooth muscle requires oxygen to remain contracted
describe reactive hyperemia
when tissue blood flow is blocked for some reason
- after unblocked
- tissue flow increases 4-7x normal because this tissue went w/o nutrients
describe active hyperemia
when a tissue becomes active, such as exercise
the rate of blood flow to that tissue will increase
increase in metabolism vs. tissue blood flow
increased metabolism = increased flow
effect of decreased arterial oxygenation saturation on blood flow
when o2 levels decrease = blood flow increases
autoregulation
- 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
theories to explain autoregulation
- metabolic theory
2. myogenic theory
describe metabolic theory of autoregulation
increased blood flow
=too much o2 to tissues
= washes out vasodilators
= vasodilation to reduce flow when tissues are satisfied
describe myogenic theory of autoregulation
increased blood flow
= stretching of vessels
= reactive vasculature constriction
= reduced flow in response to stretching of vessels
special acute blood flow control mechanisms exist in the: ?
kidneys
brain
skin
kidney acute blood flow control
tubuloglomerular feedback – kidney tubules monitor flow and have special mechanisms to allow them to effect flow
brain acute blood flow control
increased co2 (also increased [H+])
=cerebral vessel dilation
=causes washing out of excess co2/H+
skin acute blood flow control
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)
endothelium derived mechanism for blood flow control
healthy endothelial cells release NO
=which converts cGTP to cGMP
=cGMP activates protein kinases
=kinases are vasodilators
how does hypertension effect endothelium control of blood flow
inhibits the release of NO
-so endothelium cannot induce vasodilators
blood flowing thru arteries and arterioles causes ____ stress which leads to endothelium releasing ____ .
shear stress
release of NO
list vasoconstrictors of humoral control
- norepinephrine
- epinephrine
- angiotensin II
- vasopressin
what is ADH
anti-diuretic hormone
causes the retaining of fluids
angiotensin II
vasoconstriction
acts to increase total peripheral resistance
vasopressin
vasoconstrictor
also called ADH
very powerful vasoconstrictor
major function is to control body fluid volume
humoral circulation control: vasodilators
- bradykinins
2. histamine
bradykinins
cause both vasodilation and increased capillary permeability
histamines
powerful vasodilator derived from mast cells and basophils
sympathetic system: circulation
- innervates all vessels except capillaries
2. stimulation primarily results in vasoconstriction
what secretes epinephrine and norepinephrine
adrenal medulla
list the vasomotor centers in the brain
- vasoconstriction area
- vasodilation area
- sensory area
- other
vasoconstriction area in brain
- upper medulla
2. transmits continuous signals to BVs
vasomotor tone
= partial state of contraction of blood vessels
vasoconstrictor area continuous firing
results in sympathetic vasoconstrictor tone
vasodilator area of brain
lower medulla
inhibits vasoconstrictor area activity
sensory area of brain vasomotion
in medulla and both sides of brain
receives signals from vagus and glossopharyngeal nerves
other areas of vasomotor control in brain
- brain stem (reticular substance)
- hypothalamus
- cerebral cortex
baroreceptors in carotids and aorta
inhibit vasoconstrictor center and stimulate vasodilator center
carotid bodies
present in aorta and carotids
- chemosensitive cells
- more important for respiratory control
neural rapid control of atrial pressure
- cause simultaneous changes
- rapid response w/in seconds
- ex. increased blood pressure during exercise, flight or fight responses
what changes can the brain induce to control atrial pressure
simultaneous changes
- constriction of most systemic arteries
- constriction of veins
- increased heart rate
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
baroreceptors
- pressure receptors stimulated by low arterial pressure
- located in aorta and carotids
- vagus nerves
- glossopharyngeal nerves
baroreceptors pressure limits
aorta - press > 80-200
carotid - press > 60-180
other locations of baroreceptors
reticular substance
hypothalamus
cerebral cortex
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
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
reflex dilation of kidney afferent arterioles
increases kidney fluid loss
decreases blood volume
decreases pressure
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
ANP
sends signals to kidneys
increase GFR
decrease Na+ absorption
to increase fluid loss
an atrial reflex in response to stretching
what is the result of decreasing Na+ absorption
cells don’t absorb Na so it is lost to urine
arterial pressure =
CO x total peripheral resistance
arterial pressure rises when
total peripheral resistance is acutely increased
normal functioning kidneys return arterial pressure back to normal w/in few days
normal kidney function is capable of maintaining normal arterial pressure even as ….
CO ranges from 40 - 160% of normal output
primary or essential hypertension
- unknown origin
- 90-95% of hypertension
- major factors: weight gain and sedentary lifestyle
secondary hypertension
- hypertension second to some other cause
- examples: tumors, renal artery constriction, preeclampsia, neural, genetic
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
factors resulting in decreased peripheral resistance = decreased BP
- increased production of NO, release of prostacyclin and kinins and ANP
- decreased neural factors
factors resulting in decreased cardiac output leading to decreased BP
-decreased blood vol., HR, contractility of heart
vasoconstrictors
angiotensin II
catecholamines
endothelin
vasodilators
kinins
prostaglandins
NO
lethal effects of chronic hypertension
- early heart failure and coronary artery disease
- cerebral infarction
- kidney failure
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
non-modifiable risk factors of atherosclerosis
- age
- gender
- genetics
define hyperhomocystinemia
inborn error of metabolism
pathogenesis of atherosclerosis
- endothelial injury or dysfunction of any kind
- accumulation of lipoproteins
- monocyte adhesion to endothelium
atheroma morphology
- consists of a cap of smooth muscle cells, macrophages, foam cells, and other extracell components
- this occurs within the vessels
early stage of atherosclerosis
- early lesions are fatty streaks
- plaques forming white/yellow
- plaques can be calcified, rupture or erode
common sites of atherosclerosis
- lower aorta
- coronary art.
- carotid art.
convert macrophages
foam cells
long term control of arterial pressure
- nervous and hormone control
- kidneys
relate urinary output and arterial pressure
positive correlation
pressure diuresis
increase urine output
pressure natriuresis
increase sodium output
near infinite feedback gain principle
return of arterial pressure back to equilibrium point
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
acute increases in blood pressure cause 2-3x increase in _____ ____ output. which is independent of ______ .
urinary Na output
independent of sympathetic system of hormones
over a long period, water and salt ____ must equal _____ .
output = input
increased intake of salt and water increases?
arterial pressure
via kidney function
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
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)
define chronic hypertension
one’s mean arterial pressure is greater than the upper range of the accepted normal measure
aka chronic high blood pressure
normal vs hypertensive vs. severe hypertensive BP
90 – 110/70
110 – 135/90
150 – 250/130
(90 = mean pressure)
lethal effects of chronic hypertension
- early heart failure
- coronary heart disease
- MI
- cerebral infarct
- kidney failure
destruction of areas of kidneys
= kidney failure
= uremia
=death
renin-angiotensin system
something causes a decrease in blood pressure
this system works to increase pressure
steps of renin-angiotensin system
- decreased arterial press.
- effects renin sys.
- kidney releases renin
- angiotensinogen converted to angiotensin I
- angiotensin I converted to angiotensin II
- II acts
- bp increased
effects of angiotensin II
- on kidneys to retain salt and water
- acts on adrenal gland to release aldosterone
- vasocontriction
- inactivate angiotensinase
what does renin do?
the liver produces angiotensinogen
renin converts this to angiotensin I
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
renin-angiotensin system for increased salt intake
- increase Na intake
- increased Extracellular fluid vol.
- increased arterial press.
- decreased renin and angiotensin
- decreased renal retention
- return of extra fluid to normal
- arterial pressure return to normal
ACE
angiotensin converting enzyme
