Chapter 19.
Vessels and Circulation
BIOL242
Lab Pracicum Weds.?
• On Chap 16 – 19 (Endocrine &
Cardiovascular Lab)
• Lab Practical, 24 Oct. Weds on 16 -19
(Lab schedule says “No Lab Scheduled”)
Overview
• Classes of blood vessels and their
structures
• Cardiovascular physiology
• Circulatory pressures
• Capillary exchange
• Cardiovascular regulation
• Vascular diseases
• Vessels to know (repeat from lab)
Blood Vessels
•
Closed system of tubes that starts and ends at
the heart
Arteries: large vessels that carry blood away from
heart
Arterioles: smallest branches of arteries
Capillaries: smallest blood vessels with a small
diameter and thin walls; location of exchange
between blood and interstitial fluid (exchange
vessels)
Venules: smaller branches of veins collect blood
from capillaries
Veins: Larger vessels that return blood to heart
Structure of Vessel Walls
Figure 21-1
Generalized Structure of Blood
Vessels
• Arteries and veins are composed of three
tunics – tunica interna, tunica media, and
tunica externa
• Lumen – central blood-containing space
surrounded by tunics
• Capillaries are composed of endothelium
with sparse basal lamina
Artery and Vein Walls – 3 layers
• Tunica Interna (Intima): innermost layer
– endothelial lining of all vessels
– In vessels larger than 1 mm, a subendothelial
connective tissue basement membrane is present
– In arteries only the internal elastic membrane is a
layer of elastic fibers in outer margin
• Tunica Media: middle layer
– concentric sheets of smooth muscle in loose
connective tissue
– regulated by sympathetic nervous system
– Controls vasoconstriction/vasodilation of vessels
– External elastic membrane (arteries only) separates
tunica media from tunica externa
– Thickest layer in a small artery
Artery and Vein Walls – 3 Layers
• Tunica Externa (adventitia): outer layer
–
–
–
–
Connective tissue sheath with collagen fibers
Anchors vessel to adjacent tissues
Thick in veins
Larger vessels contain vasa vasorum
• In arteries:
– collagen fibers
– elastic fibers
• In veins:
– elastic fibers
– smooth muscle cells
Vasa Vasorum
• Small arteries and veins found in the walls
of large arteries and veins
• These are the blood supply for the large
vessels
• Supply cells of tunica media and tunica
externa with oxygen and nutrients
• Why don’t you need these in capillaries?
Arteries vs. Veins at a glance
• Arteries and veins run side-by-side
• Arteries have thicker walls and higher blood
pressures
• Collapsed artery has small, round lumen
• Vein has a large, flat lumen
• Vein lining contracts, artery lining does not
• Artery lining folds
• Arteries more elastic
• Veins have valves
• Arteries thick t. media, veins thick t. externa
Vessel Composition
Arteries
• Elasticity allows arteries to absorb
pressure waves that come with each
heartbeat
• Contractility: arteries change diameter,
controlled by sympathetic division of ANS
– Vasoconstriction: contraction of arterial
smooth muscle by the ANS, shrinking lumen
– Vasodilation: The relaxation of arterial smooth
muscle, enlarging lumen
Vasoconstriction
and Vasodilation
• Active processes that affect:
– afterload on heart (how?)
– peripheral blood pressure (how?)
– capillary blood flow
Note: elasticity of the arteries also allows
them to expand and contract passively in
response to changes in blood pressure
Structure
of Blood
Vessels
Figure 21-2
Vascular
Components
Artery Characteristics
• From heart to capillaries, arteries change characteristics
(along a continuum):
– Elastic arteries (conducting arteries)
• Large vessels (e.g. and aorta) dmax = 2.5cm, lumen allow lowresistance conduction of blood
• Contain elastin in all three tunics
• Withstand and even out large blood pressure fluctuations
• Serve as pressure reservoirs
• Tunica media has many elastic fibers and few muscle cells
– Muscular arteries (distribution arteries)
•
•
•
•
Medium-sized davg =0.4cm
Account for most arteries
Thick tunica media has many muscle cells
Active in vasoconstiction
– Arterioles (resistance vessels)
• Smallest arteries (d ≤ 30 micons)
• Have little or no tunica externa, thin or incomplete media
• Control blood flow into capillaries by change diameter in response
to ANS, local conditions
Artery Diameter and Resistance
• Small muscular arteries and arterioles
change diameter with sympathetic or
endocrine stimulation (vasomotor response)
– Decreasing diameter increases resistance,
the force opposing blood flow
– Arterioles also called resistance vessels
Aneurysm
• Bulge in an arterial wall
• Caused by weak spot in elastic fibers
• Pressure may rupture vessel
Capillaries
• Are smallest vessels with thin walls (davg = 8
microns)
• We have about 10 billion or 25,000 miles
• Have only a tunica interna, one cell thick
• Pericytes on the outer surface stabilize their
walls
• Microscopic capillary networks permeate all
active tissues
• Blood flow through caps is slow (why?)
• Exchange occurs here: materials diffuse
between blood and interstitial fluid
• All living cells no more than 125 um from a cap
3 Types of Capillaries
• Continuous
– Abundant in skin and muscles
– Have complete endothelial lining, connected by tight junctions
– Small clefts permit diffusion of water, small solutes, and lipid soluble
material (but NOT blood cells or plasma proteins)
– thymus and brain have specialized continuous capillaries (barriers)
• Fenestrated
– Have pores in endothelial lining (not gaps between cells)
– Permit more rapid exchange of water and larger solutes between
plasma and interstitial fluid
– Found in: choroid plexus, kidneys, intestinal tract, and?
• Sinusoids
– Modified fenestrated capillaries
– Very leaky, with large gaps between adjacent endothelial cells that allow
large molecules (plasma proteins) and cells through
– Found only in: Liver, spleen, bone marrow, other lymphoid tissues, used
for phagocyte monitoring, plasma protein entry from liver
Capillary Structure
Figure 21-4
Capillary Networks
• One arteriole gives rise to several capillary
beds
• Each Capillary bed connects 1 arteriole to 1
venule
• Each capillary entrance guarded by
precapillary sphincter
Capillary Bed – key parts
• Capillaries
– 10 to 100 capillaries per capillary bed, they branch off the
metarteriole and return to the thoroughfare channel at the distal
end of the bed
• Thoroughfare Channels
– Are direct capillary connections between arterioles and venules
– Controlled by smooth muscle segments called metarterioles
found at channel entrance
• Collaterals
– Multiple arteries contribute to one capillary bed and allow
circulation if one artery is blocked
– Arterial anastomosis = fusion of two collateral arteries
• Arteriovenous Anastomoses
– direct connections between arterioles and venules allow blood to
bypass the capillary bed
Capillary Networks
Figure 21-5
Precapillary Sphincters
• Guards entrance to each capillary
• Open and close, causing capillary blood to flow in
pulses
• Vasomotion:
– Contraction and relaxation cycle of capillary
sphincters
– Causes blood flow in capillary beds to constantly
change routes
– Contract/relax on the order of 10 times/min
– Causes capillary flow to pulse
– Controlled by autoregulation (see later)
Closed precapillary sphincters
Capillary Volume
• At rest, blood is flowing in about 25% of
your capillaries
• When you begin to exercise, vessels must
redistribute blood within the capillary
network (you can’t just open up more
capillaries)
• If all your capillaries open at once: shock
Veins
• Collect blood from capillaries in all tissues
and organs and return it to heart
• Larger in diameter than arteries, but have
thinner walls and much lower blood
pressures
• Tunica externa is usually thickest layer
• Capacitance vessels (blood reservoirs)
that contain 65% of the blood supply
• Classified on the basis of size
Vein Characteristics
• Venules
– Collect blood from capillaries
– Average diameter of 20 um, resemble capillaries in structure
– Allow fluids and WBCs to pass from the bloodstream to tissues
• Medium Sized Veins
– thin tunica media and few smooth muscle cells
– Thickest part is tunica externa with longitudinal bundles of elastic
fibers and collagen
– Size ranges from 2 – 9 mm
• Large Veins (e.g. sup/inf vena cava)
– have all 3 tunica layers
– thick tunica externa with thin tunica media
Vein Valves
•
•
•
•
Valves are folds of tunica interna
Resemble semilunar heart valves
Prevent blood from flowing backward
Compression from muscular contractions (even
rotation in isometric contractions) pushes blood
toward heart
• Not so important when lying down
• Compartmentalize blood flow: blood return from
below heart is like a boat traversing several
locks to get up a hill
Valves in the Venous System
Figure 21-6
Blood
Distribution
Figure 21-7
Blood Distribution
• Heart, arteries, and capillaries:
– 30 – 35% of blood volume
• Venous system:
– 60 – 65%
– Fully ⅓ of venous blood is in the large venous
networks of the liver, bone marrow, and skin
(some of this is part of the venous reserve)
Capacitance
• The ability to stretch or the relationship
between blood volume and blood pressure
• Veins (capacitance vessels) stretch more
than arteries (8x as much as arteries)
• Lower resistance = higher capacitance =
expands easily at low pressures
• Means veins can accommodate large
changes in blood volume
Veins Response to Blood Loss
• Vasomotor centers (medulla) stimulate
sympathetic nerves
• Venoconstriction = smooth muscles in
systemic medium sized veins constrict
• Affects blood pressure in venous system
but major effect is to cause veins in liver,
skin and lungs to redistribute venous
reserve back to arterial system (about
20% of total blood)
Cardiovascular Physiology
Figure 21-8
Cardiovascular Physiology
• Cardiac output = blood flow
– Determined by pressure and resistance in the
cardiovascular system
– Force is proportional to pressure gradient
resistance
• Pressure (P) = force the heart generates to
overcome resistance
• Absolute pressure is less important than
pressure gradient
• Pressure Gradient (P) = the difference between
pressure at the heart and pressure at peripheral
capillary beds
Blood Flow, Pressure, and Resistance
• Blood flow (F) is directly proportional to the
difference in blood pressure (P) between two points
in the circulation
– If P increases, blood flow speeds up; if P
decreases, blood flow declines
• Blood flow is inversely proportional to resistance (R)
– If R increases, blood flow decreases
• R is more important than P in influencing local
blood pressure
• The differences in pressure within the vascular
system provide the driving force that keeps blood
moving, always from higher to lower pressure area
Measuring Pressure
• Blood pressure (BP):
– arterial pressure (mm Hg)
– Pressure required to move blood
• Capillary hydrostatic pressure (CHP):
– pressure within the capillary beds
– pressure where diffusion and osmosis occur
• Venous pressure:
– pressure in the venous system
• Circulatory Pressure: ∆P across the systemic
circuit (about 100 mm Hg)
Resistance
• Resistance – opposition to flow
– Measure of the amount of friction blood encounters
– Generally encountered in the systemic circulation
– Referred to as peripheral resistance (PR)
• Circulatory pressure must overcome total
peripheral resistance of entire cardiovascular
system which comes from 3 sources:
– Vascular resistance (length and diameter)
– Blood viscosity
– Turbulence
Peripheral Resistance: vascular
resistance
• Vascular resistance (= major factor): R of
blood vessels due to friction between blood
and vessel walls depends on vessel length
and vessel diameter
– Adult vessel length is constant
– Vessel diameter varies by vasodilation and
vasoconstriction
– R increases exponentially (4th power!) as
vessel diameter decreases (double the radius,
decrease resistance by 16x)
Peripheral Resistance: viscosity and
Turbulence
• Viscosity also increases resistance
– Normal whole blood viscosity is about 4 – 5
times that of water, changes with hematocrit
• Turbulence: swirling action that disturbs
smooth flow of liquid
– Occurs in heart chambers and great vessels
– Atherosclerotic plaques cause abnormal
turbulence
Overview of Circulatory Pressures:
Arteries
• Largest pressure gradient is between aorta
and proximal end of capillary beds (100 
35 mmHg so gradient = 65)
• This part of the system also has the highest
resistance.
• Both the pressure (CO) and the resistance
(vasomotor tone) can be regulated,
determining the rate of flow in the capillaries
Overview of Circulatory Pressures:
Capillaries
• Blood at the proximal (arterial) side of cap beds
has pressure of 35 mmHg
• At distal end, where blood enters venules,
pressure is 18 mmHg
• Low capillary pressure is desirable because high
BP would rupture fragile, thin-walled capillaries
• Low BP is sufficient to force filtrate out into
interstitial space and distribute nutrients, gases,
and hormones between blood and tissues
Overview of Circulatory Pressures:
Veins
• Blood entering venules is 18 mmHg,
enters right atrium at 0 – 2 mmHg so
gradient = 18 mmHg (pretty small)
• However, veins provide very low
resistance and so they don’t require great
pressures for blood to move
• As blood gets closer to heart, veins get
larger and larger, decreasing resistance.
This doesn’t increase the pressure but it
does increase the velocity of blood flow
Systemic Blood Pressure
Figure 19.5
Vessel
Diameter
Cross-Sectional
Area
Average
Systemic
Blood
Pressure
Systemic
Blood
Velocity
What the graphs show
• Arteries  capillaries (divergence)
• Capillaries veins (convergence)
• Blood pressure and velocity are proportional to
the TOTAL cross sectional area of all vessels
• As total cross-sectional area increases, avg.
blood pressures and velocities decline
• Velocity continues to decline until the veins,
where cross sectional areas increase (reducing
friction)
• Velocity is slowest at capillaries and flow allows
adequate time for exchange between blood and
tissues
Pressures in the
Systemic Circuit
• Systolic pressure:
– peak arterial pressure during ventricular
systole
• Diastolic pressure:
– minimum arterial pressure during diastole
• Pulse pressure:
– difference between systolic pressure and
diastolic pressure
• Mean arterial pressure (MAP):
– MAP = diastolic pressure + ⅓ pulse pressure
Pressure and Distance
• MAP and pulse pressure decrease with
distance from heart
• Blood pressure decreases with friction
• Pulse pressure decreases due to elastic
rebound
• Near the heart, BP pulses
• By the arterioles, pulsing is gone (if you
cut a vein it will bleed continuously; an
artery spurts)
Elastic Rebound
• Elastic rebound = Ability of arteries to
expand and recoil
• Arterial walls:
– stretch during systole
– rebound during diastole
– keeps blood moving during diastole
• Dampens the effect of the pulse:
– By the time the blood reaches the arterioles,
flow is continuous
Abnormal Blood Pressure
• Hypertension:
– abnormally high blood pressure, greater than
140/90
– High diastolic can be very dangerous
• Hypotension:
– abnormally low blood pressure
Venous Return
• Amount of blood arriving at right atrium
each minute
• Both pressure and resistance are low in
venous system
• Venous BP alone is too low to promote
adequate blood return and is aided by
– the respiratory pump: pressure changes
created during breathing suck blood toward
the heart by squeezing local veins. Becomes
a larger factor as breathing rate increases.
– compression of skeletal muscles, pushes
blood toward heart (one-way valves)
Capillary Diffusion Routes
•
•
•
•
•
Oxygen and nutrients pass from the
blood to tissues
Carbon dioxide and metabolic wastes
pass from tissues to the blood
Water-soluble solutes pass through clefts
and fenestrations
Lipid-soluble molecules diffuse directly
through endothelial membranes
Plasma proteins cross endothelial lining
in sinusoids only
Capillary Exchange
• Capillary Exchange is fluid movement
between capillaries and interstitial space
– Capillary pressure normally forces water and
solutes OUT into the tissues
– vital to homeostasis, creates and circulates
interstitial fluid
– moves materials across capillary walls by:
• Filtration
• Reabsorption (diffusion)
Filtration
• Filtration: the removal of solutes through a
porous membrane, driven by hydrostatic
pressure
• Hydrostatic pressure = pressure exerted
by a fluid (at rest or while flowing)
• Capillary filtration: water and small solutes
forced through capillary wall, leaving
behind larger solutes in bloodstream
Capillary Filtration
Figure 21-11
Reabsorption
• Occurs via osmosis, where water enters
the solute compartment with higher
osmotic pressure
• Solutes in a solvent generate a pressure =
Osmotic pressure:
– equals pressure required to prevent osmosis
– is a pulling force generated by solutes in a
solution that cannot cross the membrane
Overview: Osmotic and
Hydrostatic Pressures
• Hydrostatic pressure:
– forces water out of a solution compartment
• Osmotic pressure:
– forces water into a solution compartment
• Balance between them controls filtration
and reabsorption through capillaries
Forces Across Capillary Walls
Figure 21-12
Hydrostatic Pressures
• Capillary hydrostatic pressure (HPc): pressure
within the capillary beds generated by heart
pumping
– Ranges from 35 at arterial end to 18 at venous end
• Interstitial fluid hydrostatic pressure (HPif):
pressure generated by mechanical force
pushing fluid back into the blood
– Different in different tissues but overall average is 0
• Net Hydrostatic Pressure (NHP): The difference
between HPc and HPif
• HPc is higher, so net pushes water and solutes
out of capillaries into interstitial fluid (this is
filtration)
Osmotic Pressures
• Capillary Colloid Osmotic Pressure (OPc) = 25
mmHg normally because suspended plasma
proteins are too large to cross capillary walls
thus they exert an osmotic pressure that pulls
water back into the capillary
– Also called oncotic pressure
• Interstitial Fluid Colloid Osmotic Pressure (OPif)
= effectively zero under normal conditions
because there is no pressure exerted by
suspended proteins outside cells
• Net Colloid Osmotic Pressure (NCOP): The
difference between OPc and OPif
• OPc is higher and so it pulls water and solutes
into capillary from interstitial fluid (this is
reabsorption)
Net Filtration Pressure (NFP)
• NFP – all the forces acting on a capillary bed
• The difference between net hydrostatic
pressure and net osmotic pressure
NFP = (NHP) – (NCOP)
NFP = (HPc – HPif) – (OPc – OPif)
NFPArt = (35 – 0) – (25 – 0) = +10 mmHg (out)
NFPVen = (18 – 0) – (25 – 0) = -7 mmHg (in)
Capillary Exchange
• At arterial end of capillary bed hydrostatic forces
dominate:
– fluid moves out of capillary into interstitial fluid =
filtration
• At venous end of capillary osmotic forces
dominate:
– fluid moves into capillary out of interstitial fluid =
reabsorption
• But what about in between?
• Transition Point = point along capillary bed
where filtration switches to reabsorption.
• If this were right in the middle, what would the
net result be (filtration, reabsorption?)
Capillary Exchange
• Since we know which one dominates
(right?) the question is, where is the
transition point?
• Closer to the arterial end or to the venous
end?
Forces Across Capillary Walls
Figure 21-12
Summary: Forces in the capillary bed
• Hydrostatic pressure tends to push water
and solutes OUT OF blood, into interstitial
fluid
• Colloid osmotic pressure tends to pull
water and solutes INTO capillary
• Net filtration pressure is the difference
between the NHP and NCOP
• At proximal end, NHP is higher
• At distal end, NCOP is higher
The Transition Point
• Transition occurs closer to distal (venous)
end, thus capillaries filter more than
reabsorb so more fluids enter the tissue
beds than return to the blood,
• Excess fluid enters interstitial space,
becomes interstitial fluid (net 3.6L/day)
• Eventually, fluid will enter lymphatic
vessels, become lymph
• Then what?
Changes in Capillary Dynamics
• Hemorrhaging:
– reduces HPc and thus NFP
– increases reabsorption of interstitial fluid (called recall
of fluids)
• Dehydration:
– increases OPc, decreases NFP
– Also accelerates reabsorption (recalls fluids)
• Increase in HPc or decline in OPc :
– Happens in starvation, heart failure
– fluid moves out of blood
– builds up in peripheral tissues (edema)
Cardiovascular Regulation
• Goal is to maintain adequate Tissue
Perfusion, blood flow through the tissues
• Carries O2 and nutrients to tissues and
organs, carries CO2 and other wastes away
• Is affected by:
– cardiac output (HR, stroke volume)
– peripheral resistance (vessel diameter)
– blood volume
• Blood pressure = CO x PR
Cardiovascular Regulation
• Changes blood flow to a specific area at
an appropriate time, without changing
blood flow to vital organs
3 Regulatory Mechanisms
• Control of cardiac output and blood pressure:
1. Autoregulation:
• causes immediate, localized homeostatic
adjustments
2. Neural mechanisms:
• respond quickly to changes at specific sites
3. Endocrine mechanisms:
• direct long-term changes
• Short-term controls counteract moment-to-moment
fluctuations in blood pressure by altering
peripheral resistance
• Long-term controls regulate blood volume
Cardiovascular Responses
Figure 21-13
1. Autoregulation
• Local blood flow within tissues is adjusted
by peripheral resistance while cardiac
output stays the same (no effect on heart)
• Vasodilators: dilate precapillary sphincters
– Local vasodilators: accelerate blood flow at
tissue level:
•
•
•
•
•
•
Low O2 or high CO2 levels
Low pH (acids)
Nitric oxide (NO)
High K+ or H+ concentrations
Chemicals released by inflammation (histamine)
Elevated local temperature
Autoregulation
• Local Vasoconstrictors
– e.g. prostaglandins and thromboxanes
released by damaged tissues
– constrict precapillary sphincters
– affect a single capillary bed
At high concentrations, both local
vasodilators and vasoconstrictors may
also affect arterioles (which would affect
many capillary beds)
2. Neural Mechanisms
• Cardiovascular (CV) centers: vasomotor center
plus the cardiac centers of medulla oblongata that
integrate blood pressure control by altering cardiac
output and blood vessel diameter (adjusts cardiac
output and peripheral resistance)
–
–
–
–
Vasomotor center: adjust size of arterioles
Cardioacceleratory center: increases cardiac output
Cardioinhibitory center: reduces cardiac output
All are part of sympathetic nervous system
• Neural controls of peripheral resistance:
– Alter blood distribution in response to demands
– Maintain MAP by altering blood vessel diameter
Neural: Vessels
Vasomotor Center
• Vasomotor center – a cluster of sympathetic neurons in
the medulla that oversees changes in blood vessel
diameter
– Maintains blood vessel tone by innervating smooth muscles of
blood vessels, especially arterioles
• Vasoconstriction
– controlled by adrenergic nerves (NE)
– stimulates smooth muscle contraction in arteriole walls
– neurons innervate peripheral blood vessels throughout body
• Vasodilation:
– controlled by special sympathetic nerves
– relaxes smooth muscle
– neurons found only in skeletal muscles and heart
Vasomotor Center
• Vasomotor tone: constant action of sympathetic
vasoconstrictor nerves keep arterioles
constricted to a point about halfway between
fully dilated and fully constricted
• Modest adjustments can make huge changes in
peripheral resistance, and thus in arterial blood
pressure
• Extreme widespread sympathetic stimulation
causes venoconstriction too, a narrowing of
systemic veins to mobilize the venous reserve
Vasomotor Control
• For most peripheral tissues the
sympathetic nervous system affects the
state of the arterioles: at rest, sympathetic
tone keeps them in the middle of their
possible openness.
– If BP drops, sympathetic activity increases
and vasoconstriciton occurs
– If too high, sympathetic activity declines and
vasodilation occurs
– Parasympathetic NS does not play a role
Cardiovascular centers
• Baroreceptors and chemoreceptors
monitor arterial blood composition and
pressure and signal the cardiovascular
centers to change
Baroreceptor Reflexes
• Baroreceptor reflexes: stretch receptors in walls
of the carotid sinuses, aortic sinuses, and right
atrium responds to changes in blood pressure:
• When blood pressure rises, increased
stimulation to cardiovascular centers causes
them to:
– decrease cardiac output
– cause peripheral vasodilation
• When blood pressure falls, less stimulation to
cardiovascular centers causes them to:
– increase cardiac output
– cause peripheral vasoconstriction
Impulse traveling along
afferent nerves from
baroreceptors:
Stimulate cardioinhibitory center
(and inhibit cardioacceleratory center)
Baroreceptor
Reflexes
Baroreceptors
in carotid
sinuses and
aortic arch
stimulated
Sympathetic
impulses to
heart
( HR and contractility)
CO
Inhibit
vasomotor center
R
Rate of vasomotor
impulses allows
vasodilation
( vessel diameter)
Arterial
blood pressure
rises above
normal range
CO and R
return blood
pressure to
Homeostatic
range
Stimulus:
Rising blood
pressure
Homeostasis: Blood pressure in normal range
Stimulus:
Declining
blood pressure
CO and R
return blood
pressure to
homeostatic
range
Peripheral
resistance (R)
Vasomotor
fibers
stimulate
vasoconstriction
Impulses from
baroreceptors:
Stimulate cardioacceleratory center
(and inhibit cardioinhibitory center)
Cardiac
output
(CO)
Sympathetic
impulses to heart
( HR and contractility)
Arterial blood pressure
falls below normal range
Baroreceptors in
carotid sinuses
and aortic arch
inhibited
Stimulate
vasomotor
center
Figure 21-14
Chemoreceptor Reflexes
• Chemoreceptors in carotid bodies and
aortic bodies
– monitor blood for changes in pH, O2, and CO2
concentrations
• Reflexes produced by coordinating
cardiovascular and respiratory activities
3. Hormonal Regulation
• Hormones have short-term and long-term effects
on cardiovascular regulation
– E and NE, hormones produced by adrenal medullae
(neuroendocrine) increase BP
– Antidiuretic hormone (ADH) – causes intense
vasoconstriction in cases of extremely low BP
– Angiotensin II – kidney release of renin generates
angiotensin II, which causes vasoconstriction
– Erythropoietin (EPO) increases blood volume and
pressure
– Natriuretic peptides (ANP, BNP) decrease blood
volume and pressure
Antidiuretic Hormone (ADH)
• Released by posterior lobe of pituitary in
response to reduced blood volume, an
increase in blood oncotic pressure, or to
Angoiotensin II release
– Elevates blood pressure (mild
vasoconstrictor)
– Reduces water loss at kidneys to increase
blood volume
Angiotensin II
• Responds to fall in renal blood pressure
• Renin – angiotensin system results in its
production by ACE in lung capillaries
–
–
–
–
–
Increases aldosterone
Increases ADH
Induces thirst
Increases cardiac output
Vasoconstritor (arterioles)
• Effect on BP is 4 - 8 times greater than NE
• Think about what that means for blood pressure
drugs (ACE inhibitors versus Beta blockers)
Erythropoietin (EPO)
• Released at kidneys
• Responds to low blood pressure, low O2
content
• Stimulates red blood cell production
ANP and BNP
• Atrial natriuretic peptide (ANP):
– produced by cells in right atrium
• Brain natriuretic peptide (BNP):
– produced by ventricular muscle cells
• Respond to excessive diastolic stretching
• Lower blood volume and blood pressure by:
– blocking ADH, aldosterone, E and NE and stimulating
peripheral vasodilation
• Reduces stress on heart
Hormonal
Regulation
Figure 21-16
CV Response to: Light Exercise
• Local vasodilation (capillaries): local
changes in oxygen cause release of local
vasodilators
• Increased venous return from increased
skeletal muscle contractions and
increased respiratory rate (resp. pump)
• Cardiac output rises to 2 times resting
levels due to increased venous return
(Frank-Starling principle) and atrial reflex
• A little sympathetic activation
CV Response to: Heavy Exercise
• General sympathetic activation
• Major redistribution of blood to muscles
due to dilation there and constriction
everywhere else
• Cardioaccelaratory centers increase HR,
increase CO, so blood moves through the
system more quickly
Vascular pathology
BIOL242
Hemorrhage
• Short term problem: maintain blood
pressure and flow
• Long term problem: restore normal blood
volume
Responses to Blood Loss
Figure 21-17
Short-Term
Responses to Hemorrhage
• To prevent drop in blood pressure baroreceptor
reflexes:
– increase cardiac output (increasing heart rate)
– cause peripheral vasoconstriction
• Sympathetic nervous system:
– further vasoconstriciton constricts arterioles
– venoconstriction improves venous return if necessary
• Hormonal effects:
– increase cardiac output
– increase peripheral vasoconstriction (E, NE, ADH,
angiotensin II)
• Kidneys filter less, make less urine
Long-Term
Responses to Hemorrhage
•
Restoration of blood volume can take
several days:
1. Recall of fluids from interstitial spaces
(caused by decline in CHP)
2. Aldosterone and ADH promote fluid
retention and reabsorption
3. Thirst increases, replaces “borrowed” fluid
4. Erythropoietin stimulates red blood cell
production
Kidney and blood pressure
Shock
• Short-term responses compensate up to
20% loss of blood volume
• Failure to restore blood pressure results in
circulatory shock
• Certain after 30 – 35% blood loss
Circulatory collapse
• When arterioles and precapillary
sphincters can no longer vasoconstrict
despite the vasomotor stimulation to
elevate blood pressure
• Widespread peripheral vasodilation
• Leads to fatal decline in BP
• This is the endpoint of all types of shock if
untreated
Newborn Heart
• Before Birth
– Fetal lungs are collapsed
– O2 provided by placental circulation
• At Birth
– Newborn breathes air
– Lungs expand
– Pulmonary circulation provides O2
The Neonatal Heart
Figure 21-33b
Cardiovascular Changes at Birth
•
•
•
Pulmonary vessels expand
Reduced resistance allows blood flow to
pulmonry circuit
Rising O2 causes ductus arteriosus
constriction
• short vessel that connects pulmonary and
aortic trunks in fetus
•
Rising left atrium pressure closes
foramen ovale
Congenital
Cardiovascular Problems
Figure 21-34
Congenital
Cardiovascular Problems
• PFO – Left to right shunt
• Patent ductus arteriosus – right to left shunt, can
lead to cyanosis
• Ventricular septal defects (common) – causes
mixing of ventricular blood similar to PFO
• Tetralogy of Fallot – narrow pulmonary trunk,
incomplete IV septum, aorta originates in middle
of defective septum, RV is enlarged
• Transposition of great vessels
Arteriosclerosis
• Thickening of arterial walls, leads to coronary
artery disease (CAD), peripheral artery disease,
and stroke
– Calcification: t. media smooth muscle
replaced by calcium
– Atherosclerosis: lipid deposits form in t. media
• High levels of lipids in blood lead to phagocytosis
of lipid particles plaques clot formation
• Common in familial hypercholesterolemia
• How do plaques increase vascular resistance
(and thus afterload) in in two ways?
Antihypertensive medications
• Calcium channel blockers – negative
inotropic effect, may slow conduction
• Beta blockers – blocks sympathetic effects
on heart, vessels
• Diuretics – lower blood volume
• Vasodilators – lower BP
• ACE inhibitors
Edema
• Tissue swelling
• Caused by disruptions in balance of hydrostatic
and oncotic forces
• Capillary damage: OPif increases as plasma
proteins leak out, reduces reabsorption 
swelling at injury site
• Starvation: decreased plasma protein synthesis,
reduced OPc, edema in abdominopelvic cavity
(ascites)
• Most common in US: increase in HPc due to high
afterload (CHF, atherosclerosis, etc.)
Vessels
Vessels - Generalities
• Peripheral distributions are the same on
the left and right side of the body except
near the heart.
• Most arteries and veins follow similar
paths and are often similarly named
• One vessel can have several names (like
a street)
• Many tissues are serviced by several
arteries and veins
Veins - Generalities
• Veins are far more variable from person to
person than arteries
• Several veins, especially in the limbs,
have superficial and deep routes.
Superficial route usually only caries 10 15% of blood at a maximum and serves to
aid in thermoregulation
Vessels to know
• Be able to identify the following arteries/veins on
a model: inferior and superior vena cava, left
and right pulmonary arteries and veins, common
carotid, subclavian, brachiocephalic, coronary
• thoracic and abdominal aorta, celiac, renal,
axillary, brachial, radial, ulnar, mesenteric, iliac,
peroneal, femoral, popliteal, tibial, jugular, celiac,
splenic, gastric, hepatic and saphenous.
Major
Systemic
Arteries
Figure 21-20
Branches of the Aortic Arch
• Deliver blood to head and neck:
– brachiocephalic trunk
• right subclavian artery
• right common carotid artery
– left common carotid artery
– left subclavian artery
Arteries of
Upper Limbs
Subclavian  axial
 brachial  splits
into radial, ulnar
3D Peel Away
Descending
aorta thoracic
aorta 
abdominal aorta
 common iliac 
to be continued
renal
3 Unpaired Branches
of the Abdominal Aorta
• Celiac trunk, divides into:
– left gastric artery
– splenic artery
– common hepatic artery
• Superior mesenteric artery
• Left mesenteric artery
celiac
hepatic
gastric
splenic
mesenteric
iliac
Iliac  femoral 
popliteal Posterior
and anterior tibial.
Posteror tibial
gives rise to
peroneal
(fibular)
Veins
• Know the veins with the same names as
arteries
• Exceptions:
– saphenous (leg) no comparable artery
– jugular (neck) like carotid arteries