Blood, Blood Vessels

& Circulation

21-1
 Cardiovascular System

Blood vessels: Types

A. Arteries
-carry oxygenated blood (most of the time)
away from the heart
-thicker than veins
-arteriole = small artery

C. Capillaries
-site of gas exchange with tissues
-connect arterioles and venules
-network of microscopic vessels
(one cell thick) = capillary bed
-site of exchange: gases, nutrients,
wastes
-can be closed off when not needed
B. Veins
-carry deoxygenated blood (most of
the time) – toward the heart
-same three layers as arteries
-thinner and more expansive than
arteries
-contain valves - to help the flow
of blood back to heart
-small vein = venule
21-2
21-3
• Tunica interna (intima)
– simple squamous epithelium known
Arteries
as endothelium
– basement membrane
– internal elastic lamina
• Tunica media
– circular smooth muscle & elastic
fibers
– smooth muscle is innervated by
sympathetic nervous system
– decrease in stimulation or presence
of certain chemicals causes • Elastic Arteries
vasodilation – Largest-diameter arteries have lot of
– increase in stimulation causes elastic fibers in tunica media
muscle contraction or – Help propel blood onward despite ventricular
relaxation (stretch and recoil -- pressure
vasoconstriction reservoir)
• Tunica externa • Muscular Arteries
– elastic & collagen fibers – Medium-sized arteries with more muscle than
elastic fibers in tunica media
– Capable of greater vasoconstriction and
vasodilation to adjust rate of flow = distributing
arteries 21-4
 Blood Distribution
– Arterial circuit

• Muscular Arteries
– capable of vasoconstriction and
vasodilation
– capable of changing the
distribution of blood into tissues
– known as distributing arteries

21-5
Blood flow & Pressure gradients

• blood flow is fastest in the arteries

– slows within arterioles
– slowest rate in capillaries - allows for
exchange
– blood flow becomes faster when vessels
merge to form veins
• flow rate through a vessel is
proportional to the pressure gradient
and inversely proportional to the
vascular resistance (diameter of a
vessel)
– F = ΔP/R
• F = flow rate
• ΔP = pressure gradient
• R = resistance R = 1/r4
 constant R
Blood flow & Pressure gradients

• ΔP is the pressure gradient = difference in P between

the beginning and end of a vessel
– this is what determines flow rate – NOT the absolute
pressure!
– if there is no difference in the ΔP – i.e. no difference in
pressure at the start of the vessel and at the end of the
vessel – F will stay the same

F = ΔP/R
 Blood flow & Vessel constant ΔP

Resistance

• if ΔP remains the same to change Flow rate

you change Resistance
• R increases as r decreases – F will decrease (if ΔP
stays the same)
• R decreases as r increases – F will increase (if ΔP
stays the same)

• R depends on one major factor:

• vessel radius (r) – major determinant of R

– To overcome the effects of

increased R - you have to
increase ΔP (increase the
pressure at the start of the
vessel)
Blood flow & Viscosity
– To increase F you can increase ΔP or you can decrease R
– To decrease F you can decrease ΔP or you can increase R
– this relationship applies to non-viscous fluids

• but blood is a viscous fluid

• so there will be frictional losses as blood travels through a section of vessel
• this will cause a drop in ΔP
• caused by friction between the moving fluid and the stationary wall
– blood is viscous and sticks to the vessel wall as it moves

• with a viscous fluid - Flow rate depends on two major factors:

– 1. blood viscosity (η) - # of circulating RBCs
– 2. vessel length (L)

Pouiseuille’s Law
Flow rate = η ΔP r4
8 ηL
Pouiseuille’s Law (Snooty French Guy Law)

-true description of how blood flow through our vessels

Flow rate = η ΔP r4
8 ηL

-changing the viscosity (η) of the blood does NOT change the F value (go
ahead try it!)
-but changing the L value does
-this is because thick, viscous blood “sticks” to the blood vessel wall
-so the longer the vessel – the more sticking and the slower the blood
flows

21-10
 Blood Pressure

• Pressure exerted by blood on walls of a

vessel
– depends on the volume of blood within the
vessel and the distensibility of the vessel
– caused by contraction of the ventricles
– highest in aorta
• 120 mm Hg during systole & 80
during diastole
• difference between systole and diastole
– pulse pressure

21-11
 Blood Pressure
• the volume of blood entering an artery is not the
same as the volume leaving it
– during ventricular systole – the stroke volume
leaving the artery is 1/3 of that entering the
artery
– in other words 2/3 of the blood is still in the artery
– because the artery will distend
– during diastole – the recoil of the vessel drives the
exit of the blood

21-12
 Evaluating Circulation
• Pulse is a pressure wave
– alternate expansion & recoil of elastic artery after each systole
of the left ventricle
– pulse rate is normally between 70-80 beats/min
• tachycardia is rate over 100 beats/min/bradycardia under 60
• Measuring blood pressure with sphygmomanometer
– Korotkoff sounds are heard while taking pressure
– systolic blood pressure from ventricular contraction
– diastolic blood pressure during ventricular contraction
• provides information about systemic vascular resistance
– pulse pressure is difference between systolic & diastolic
– normal ratio is 3:2:1 -- systolic/diastolic/pulse pressure

21-13
Measuring Blood pressure

21-14
 Mean Arterial Pressure (MAP)
• mean arterial pressure – average pressure driving blood
forward into the tissues throughout the cardiac cycle
– at resting heart rate – about 2/3 of the cardiac cycle is spent in
diastole
– MAP = diastolic pressure + 1/3 (systolic – diastolic pressure)
– OR MAP – 2/3 diastolic pressure + 1/3 systolic pressure
• with a standard pressure of 120/80 – MAP is 93 mmHg
exiting the heart
• MAP falls steadily in systemic circulation with distance
from left ventricle
– 35 mm Hg entering the capillaries
– 0 mm Hg entering the right atrium

21-15
 Mean Arterial Pressure (MAP)
• our bodies need to control MAP – to keep it in a
narrow range
– we do this a few ways:
• 1. elastic arteries help decrease pressure in them through
distension
• 2. muscular arteries can vasodilate/vasoconstrict and change
the pressure in them by changing vessel radius
• 3. we can also decrease the SV of the heart

21-16
Mean Arterial Pressure (MAP)
– F = ΔP/R applies to the entire circulatory
system in addition to a single vessel
– F = cardiac output
– ΔP = MAP (ΔP = difference in pressure at the
beginning of the systemic circulation and the
end of the systemic circulation)
– R = total peripheral resistance = total
resistance offered by all systemic peripheral
vessels
– rearrange the equation - ΔP = F X R
– OR
– MAP = CO X TPR (total peripheral
resistance) 21-17
• 1 – MAP depends on CO and total peripheral resistance
• 2 – CO depends on heart rate and SV
• 3 & 4– heart rate depends on balance between the parasympathetic and sympathetic divisions of the ANS
• 5 – SV increases in response to sympathetic activation (extrinsic control)
• 6 – SV also increases with increasing venous return (intrinsic control)
• 7- 10 – venous return is increased by sympathetic induced vasoconstriction (7), skeletal muscle activity (8),
respiratory pump/activity (9) and cardiac suction (10)
• 11 – 13 – venous return is also influenced by how much blood volume returns to the heart (11), blood plasma volume
(balance between passive bulk-flow fluid exchange between plasma and ECF (12), water and salt balance (13) and
hormonal control (14)
• 15 & 16 – MAP is also determined by radius of the vessel (15) and the number of RBCs/viscosity (16)
• 17 - 20– arteriole radius can be controlled by metabolic factors which control blood need (17) - which
leads to vasodilation (18) ALSO by sympathetic activity (19) which can cause vasoconstriction (20) OR
hormonally (20)
 Arterioles
• major resistance vessels in the vascular tree
• radius is small enough to offer resistance to flow
• high arteriolar resistance causes a marked drop in the MAP as
blood flows through these vessels
– MAP arteriole entrance = 93 mm Hg
– MAP arteriole exit = 37 mm Hg
– establishes a pressure differential that encourages flow of blood into the
capillary beds within the tissue but lowers pressure enough so that it
won’t damage the capillaries
• resistance also converts the pulsatile nature of systolic-
diastolic pressure to non-pulsatile pressure within the
capillaries
• radius of the arteriole can be adjusted to
– 1. variably distribute cardiac output among the tissues/organs
– 2. help regulate arterial blood pressure
 Arterioles and Arteriolar
resistance
• vasoconstriction and vasodilation
– result of the presence of a thick layer of
smooth muscle in arterioles
– muscle is sensitive to many systemic,
local factors + neurogenic stimulation
(see yellow boxes)
• vascular tone
– arterioles normally exhibit a state of
slight constriction = vascular tone
– helps establish a baseline of arteriolar
resistance and MAP
– smooth muscle activity makes it possible
to either vasoconstrict or vasodilate
– two facets are responsible:
• 1. myogenic activity of smooth muscle
layer
– smooth muscle layer is responsive to
neural or hormonal influences AND self-
induced contractile activity
• 2. continuous release of NE by
sympathetic fibers of the ANS
21-21
 Arteriolar diameter
• Local (or intrinsic) changes – at the tissue, organ specific
– 1. local chemical factors
• metabolic factors
• vasoactive mediators
– 2. histamine
– 3. local physical factors
• hot/cold
• passive stretch of arteriole
• shear stress within arteriole
• Extrinsic factors
– 1. sympathetic nervous system
– 2. hormones

21-22
 Local Changes
• most important local chemical influences on arteriolar smooth
muscle are local changes in metabolism within that organ
• local metabolic changes can affect the diameter of an arteriole
without neural influence
• active hyperemia = local arteriolar vasodilation that increases
blood flow into an organ
– arterioles are found within an organ and can be directly affected by that organ
– during increased metabolism (e.g. increased skeletal muscle contraction)
local concentrations of chemicals change within the organ
• e.g. local concentrations of oxygen decrease as the organs begins to increase its metabolic
use of glucose
– this can result in vasodilation

21-23
 Local Changes #1: Metabolic Factors
• local metabolic factors
– decreased/increased oxygen = vasodilation/vasoconstriction
– increase carbon dioxide = vasodilation
– increased carbonic acid= vasodilation
– increased K+ - repeated APs that outpace the Na/K pump’s ability to correct
ionic changes = vasodilation
– increased osmolarity – concentration of solutes accumulates in actively
metabolic cells = vasodilation
– adenosine release – cardiac muscle – release in response to increased
metabolic activity = vasodilation
– prostaglandin release = vasodilation

• relative concentration of these factors can determine the state of

arteriolar muscle tone

• local metabolic factors cause vasodilation/vasoconstriction

through the production of vasoactive mediators 21-24
 Local Metabolic Factors Act through
Vasoactive Mediators
• these local chemical changes do not act directly on smooth muscle
but act on the endothelial cells
• Endothelial cells – simple squamous epithelia cells
– found lining the inside of the arteriole and capillary
• in response to local metabolic changes - ECs release chemical
factors called vasoactive mediators
– e.g. endothelin = vasoconstriction
– e.g. nitric oxide = vasodilation by relaxing arteriolar smooth muscle
• inhibits entrance of calcium into the smooth muscle which inhibits the opening of
the foot proteins on the sarcoplasmic reticulum
 Local Changes #2: Histamine
• NOT released by metabolic changes
• NOT produce by endothelial cells
• released upon pathology
• released by connective tissue cells within the organ or by
circulating white blood cells (mast cells, basophils)
• usually released in response to organ damage
• causes vasodilation to increase blood flow and speed healing
 Local Changes #3: Local Physical factors

• application of heat or cold

– heat causes localized arteriolar vasodilation
• increases blood flow
– cold – induces vasoconstriction
• shear stress
– blood flowing over the endothelial lining creates friction = shear stress
– increase in shear stress can cause increased release of NO from the endothelial cells
– promotes vasodilation
– increased blood flow now reduces shear stress
• myogenic response to stretch
– increased MAP drives more blood into the arteriole which pushes out against the
vessel wall = passive stretch
– SO extent of passive stretch is related to the volume of blood through the vessel
• leads to vasoconstriction to reduce this blood volume
• arteriolar smooth muscle responds to passive stretch by increasing its tone through
vasoconstriction
– arterial occlusion can block blood flow and reduce myogenic stretch since the
arterioles will dilate in response
• called reactive hyperemia
 Extrinsic control over arteriolar diameter
• includes both neural and hormonal control
• sympathetic division innervates arteriolar smooth muscle everywhere except
the brain
• NO parasympathetic innervation of arteriolar smooth muscle!
– exception – ciltoris and penis

• sympathetic activity contributes to arteriolar vascular tone – through

production of norepinephrine (vasoconstrictor)
– epinephrine made by the adrenal gland is a vasodilator!

• BUT increased sympathetic activity to certain arterioles (heart and muscle)

can induce vasodilation – drops arteriolar resistance (TPR) and changes MAP

• main area of the brain to adjust sympathetic output = cardiovascular control

center
• other brain regions involved – hypothalamus
 Hormonal control
Epi and NE can cause
vasoconstriction or
• Epinephrine and Norepinephrine can be released from the vasodilation!!! depends on
adrenal medulla (sympathetic activity) or NE can be released receptor and its location
from neurons (sympathetic)

– NE binds to 1-adrenergic receptors on ALL arteriolar

smooth muscle to increase vasoconstriction
• secreted normally at a low level in your body – results
in vascular tone
• Epi can bind these receptors also – less affinity

– cerebral arterioles do NOT have 1-adrenergic receptors

!!!
• influence entirely by local physical and chemical
changes (intrinsic changes)

– Epi binds to 2-adrenergic receptors in smooth muscle in

heart and muscle arterioles to cause vasodilation

• during the “flight or fight” response - Epi is more abundant and

has more affinity for the 2-adrenergic receptors which are FIGHT
expressed in large amounts on arteriolar smooth muscle in Or
skeletal and cardiac muscle – so overall effect is of Epi FLIGHT
vasodilation to heart and skeletal muscles
21-29
 Hormonal control
• angiotensin II – converted from angiotensin I by the
enzyme ACE (produced in the lungs)
– regulates body’s salt balance
– causes the release of aldosterone from the adrenal cortex –
increased salt reabsorption
– powerful vasoconstrictor
• vasopressin (ADH) – released from the posterior
pituitary in response to changes in water volume
– drop in water content, release of vasopressin, decreased
urine volume, increased water retention
– also constriction of peripheral vessels = vasoconstrictor
– plays a role in reducing hemorrhage

21-30
Physical
Factors

Hormones

Pathology

Chemical
Factors ANS
21-31
• the sympathetic nervous system essentially
maintains an appropriate driving pressure to
each organ (i.e. MAP) but the organ itself
controls the amount of blood that actually enters
it.
• NE/sympathetic control over arteriolar vascular tone
slightly constricts most arterioles to ensure adequate
MAP throughout the systemic circuit
• BUT the organ can override the sympathetic control
using local arteriolar control mechanisms
– analogy = water pressure in pipes

21-32
– analogy – pipe carrying water
• water pressure remains constant
• differences in the amount of water
entering the beaker depends on which
valves are open and to what extent these
valves are open
• no water flows when the valve is closed
• more water flows when the valve is wide
open (low resistance) versus when a
valve is partially open (high resistance)
• so the sympathetic NS maintains the
“water pressure” (i.e. the MAP), but
each organ can control the amount of
blood that enters them
• when increased blood flows into one
organ the others must compensate by
changing their arteriolar diameter
• SO THAT MAP IS MAINTAINED
WITHIN AN APPROPRIATE
RANGE 21-33
21-34
 Regulation of BP
• Blood pressure = MAP within a small length of blood vessel
• our body uses BP to immediately determine heart rate and contraction
strength
• BP is measured constantly by baroreceptors
– changes in pressure within blood vessels
– initiates either short-term or long-term reflexes
– two major BRs: carotid sinus & aortic arch baroreceptors (mechanoreceptors)
• as the BP within the vessels increase –increases the rate of firing of the afferent neurons
within these BRs

21-35
 Regulation of BP
• role of cardiovascular center in the medulla oblongata in
regulating BP
– integrating center for information sent by the carotid and aortic
baroreceptors
– controls BP by regulating heart rate & stroke volume
– divided into two centers: vasomotor & cardiac centers alters the ratio
between sympathetic and parasympathetic activity to the heart and BVs
– Vasomotor center = specific neurons that regulate blood vessel diameter
• results in vasoconstriction of arterioles
– Cardiac center = made up of cardio-acceleratory, cardio-inhibitory
divisions
• signals sent out through vagus & cardiac accelerator nerves - changes heart rate

21-36
 Regulation of BP
• Higher brain centers such as cerebral cortex, limbic system & hypothalamus
• Hypothalamus
– osmoreceptors control salt and water balance and therefore long-term regulation
of BP
– also controls arteriole responses in fight or flight response, sexual orgasm, blushing
– controls cutaneous arterioles for temperature regulation
• Proprioceptors
– input during physical activity
• Peripheral and Central Chemoreceptors
– peripheral = out in the body - located in the carotid and aortic arteries
– central = in the medulla oblongata
– monitor concentration of chemicals in the blood (O2, CO2 and H+ions)
– increase BP by sending excitatory impulses to the cardiovascular center

21-37
Role of the ANS in Blood pressure

21-38
 Capillaries
• Microscopic vessels that connect arterioles to venules
• Found near every cell in the body but more extensive in highly active tissue
(muscles, liver, kidneys & brain)
– entire capillary bed fills with blood when tissue is active
– lacking in epithelia, cornea and lens of eye & cartilage
• Function is exchange of nutrients & wastes between blood and tissue fluid
• Structure is single layer of simple squamous epithelium and its basement membrane

21-39
• capillaries are not all open under resting conditions in most tissues - prevents the flow of
blood through the entire capillary bed
• capillaries branch from a metarteriole or directly from an arteriole
• metarterioles are surrounded by spiralling smooth muscle cells – form a precapillary
sphincter
• the sphincters are not innervated by the nervous system by still possess a high degree of
myogenic tone to contract in response to chemical factors released by the tissue
• the more metabolically active the tissue, the greater the number of capillaries fill because the
greater the number of metarterioles open
– e.g. muscle
– only 10% of the capillaries are open in resting muscle
– as the muscle increases its activity – local chemical factors change and the precapillary sphincters
open to allow more blood flow

21-40
• endothelial cells fit together like a jigsaw puzzle with considerable gaps in
between the cells = pores
– pore sizes vary from capillary to capillary
– brain capillaries have EC cells held together by tight junctions – no pores
• most tissue capillaries allow the passage of small water-soluble substances but
don’t allow the passage of larger non lipid-soluble materials
– allows the passage of glucose, small amino acids and peptides and ions
• transport may actually be regulated by the capillary itself
– endothelial cells secrete substances that “tighten” up their junctions
– histamine increases the gaps by inducing a contractile response in the EC and widening
the gaps
• in the liver, the capillary walls have larger pores to allow the passage of proteins
– liver synthesizes the plasma proteins which must be allowed to pass into the circulatory
system

21-41
 Interstitial Fluid & ECF
• there is a passive intermediary between blood plasma and the cytosol of cells =
called Interstitial Fluid (tissue fluid)
• –only 20% of the ECF circulates as blood plasma
– the remaining 80% is Interstitial Fluid
– exchange between the cytosol of the cell and the interstitial fluid is passive or active –
depending on the cell and the solute being moved
– BUT exchange between the interstitial fluid and the blood plasma is primarily
PASSIVE
• there is a limited amount of active transport = vesicular transport
– because the gaps in a capillary wall are quite large, the interstitial fluid and the
composition of the blood plasma are essentially the same

• two ways to exchange materials

between the blood and interstitial
fluid
1. diffusion
2. bulk-transport
21-42
 Diffusion
• movement of individual solutes between
blood plasma and interstitial fluid
– e.g. O2, CO2
• diffusion is promoted by several factors:
– 1. short distance of travel
• 1. thinness of the capillary wall
• 2. narrowness of the capillary
• 3. proximity to cells
– 2. total surface area – 10 to 40 billion
capillaries available for exchange

21-43
 Diffusion
– 3. velocity through the capillary
• slowest velocity is found in the capillaries
• slow velocity of flow allows for sufficient
exchange time
• velocity is inversely proportional to the
total cross-sectional area of all the vessels
at any given level of the circulatory system
• its NOT the “flow rate” – but the velocity of
the blood that determines diffusion rate
• analogy – river – lake – river
– flow rate is the volume of water flowing past
any two points in a certain amount of time
– flow rate in the river equals that of the
lake
– however, the speed/velocity of the water
flowing is slower in the lake

21-44
 X

A C
 Bulk-flow
• a volume of protein-free plasma filters out of the capillary and mixes with the
surrounding interstitial fluid and then is reabsorbed = bulk flow
• bulk flow: movement of plasma into the interstitial fluid
– the various components are moved in bulk in contrast to the movement of individual components
as seen in diffusion
• determines the composition of interstitial fluid of your tissues

• Net exchange pressure = (Pc + πIF) – (πP + PIF)

21-46
• factors affecting bulk flow
– 1. Pc = capillary blood pressure
• fluid or hydrostatic pressure exerted on the inside of the capillary wall by
blood
• “outward” force - tends to force fluid OUT of the capillaries into the
interstitial fluid
– 2. πP = plasma osmotic pressure (oncotic pressure)
• osmotic pressure encourages inward movement of fluid into the blood
plasma
• “inward” force
• doesn’t change over the length of the vessel

– 3. PIF = interstitial fluid hydrostatic pressure

• fluid pressure exerted on the outside of the capillary wall by interstitial fluid
• “inward” force
– 4. πIF = interstitial fluid-colloid osmotic pressure (πIF is close to zero)
• does not normally contribute significantly to bulk flow
• caused by the osmotic pressure of proteins in the interstitial fluid
• “outward” force

21-47
 Bulk-flow
• when blood pressure inside the capillary (Pc) exceeds that of the osmotic pressure
of the blood plasma (πP) – fluid is pushed out through the pores in the capillary
wall = ultrafiltration
– with the fluid comes the movement of multiple other components
• when inward driving osmotic pressure of the blood plasma exceeds the outward
blood pressure – net inward movement of fluid and fluid components =
reabsorption
• ultrafiltration and reabsorption are collectively known as bulk flow
• bulk flow plays a role in regulating the distribution of ECF between the circulating
plasma and interstitial fluid
• this is the way we establish the composition of our interstitial fluid

INTERSTITIAL Body cell

FLUID
Ultrafiltration
Reabsorption
Bulk Flow = Ultrafiltration – Reabsorption

Arterial end Venous

21-48end
of capillary Direction of blood flow of capillary
 Bulk-flow
• Net exchange pressure = (Pc + πIF) – (πP + PIF)
• BUT bulk flow is really determined by two major components
– 1. blood pressure/Pc
• outward driving force – from plasma to interstitial fluid
– 2. osmotic pressure of the blood/OP
• determined by the solutes within the blood plasma
• inward driving force – from interstitial fluid to plasma

INTERSTITIAL Body cell

FLUID Net fluid movement out

Blood PC decreases with blood flow

pressure OP remains the same
Osmotic
pressure

Ultrafiltration Reabsorption

Arterial end Venous end

of capillary Direction of blood flow of capillary
 Bulk-flow
• as blood flows into the capillary – the blood pressure/Pc is greater than osmotic
pressure/OP of the blood plasma (πP) and more blood plasma moves out into the
interstitial fluid then moves back in
• as blood continues to move along the capillary – Pc drops
• at the venule end of the capillary – Pc has dropped enough so that plasma OP
(πP) is now greater than Pc and more blood moves back into the plasma than is
pushed out

Bulk Flow = Ultrafiltration – Reabsorption

Ultrafiltration is driven by Pc
INTERSTITIAL Body cell
Reabsorption is driven by OPFLUID Net fluid movement out

Blood PC decreases with blood flow

pressure OP remains the same
Osmotic
pressure

Ultrafiltration Reabsorption

Arterial end Venous end

of capillary Direction of blood flow of capillary
Net exchange of fluid across capillaries
INTERSTITIAL Body cell
FLUID Net fluid movement out

Blood PC decreases with blood flow

pressure OP remains the same
Osmotic
pressure

Ultrafiltration Reabsorption

Arterial end Venous end

of capillary Direction of blood flow of capillary

21-51
 Lymph
• even under normal circumstances –
more fluid is filtered from the
blood plasma into the interstitial
fluid than is reabsorbed back into
the blood plasma
• excess fluid = lymph
• this excess fluid is directed into a
series of vessels that are similar in
structure and composition to veins
– lymphatic vessels
• one-way system of vessels that
leads back to the circulatory system
via the right lymphatic duct and the
thoracic duct

21-52
 Veins
• Proportionally thinner walls than same
diameter artery
– tunica media less muscle – little inherent
myogenic tone
– lack external elastic lamina
– tunica externa has more collagen than
elastic fibers
– strong and stretchy but possess poor elastic
recoil
• Still adaptable to variations
in volume & pressure
• Valves are thin folds of
tunica interna designed to prevent
backflow
• Venous sinus has no muscle at all
– coronary sinus or dural venous sinuses

21-53
 Blood Distribution
• 60% of blood volume at rest is in systemic veins
and venules
– function as blood reservoir
– often called capacitance vessels
– venous capacity = volume of blood the veins can
accomodate
– body at rest – much of the blood bypasses the
closed capillary beds and enters the venous return
circuit – this increases the blood volume in the
veins
– stretches the walls of the distensible veins and
allows more blood into these vessels
– but the blood moves slower than in the arteries –
lower pressure
– blood is diverted from it in
times of need
• increased muscular activity
produces venoconstriction
• hemorrhage causes
venoconstriction to help maintain
blood pressure
• 15% of blood volume in arteries & arterioles
21-54
Veins & Venules
• veins & venules have little tone and resistance
• the arteriole communicates chemically with the
venule to ensure that inflow and outflow
surrounding the capillary region matches

• venous return: volume of blood entering the atria

from the veins (pulmonary and systemic)
– much of the driving force on the blood (blood
pressure) has been lost as it enters the veins
– BP averages on 17 mm Hg in the veins
– but because the pressure of the blood entering the
right atrium in o mm Hg – there is still a small
driving force that helps to return the blood through
the veins

21-55
 Venous Return
– venous return is enhanced by many extrinsic
factors:
1. sympathetic activity – venous smooth muscle has an
abundant nervous innervation by the sympathetic nervous
division
- can produce a small amount of venoconstriction in the veins increasing venous
BP and increasing the forces driving blood back to the heart
2. respiratory activity– pressure in the chest is 5 mm Hg
less than atmospheric
– blood flowing through the veins of the thoracic cavity on the way back to the heart is
exposed to sub-atmospheric conditions
– this creates a pressure differential between the pressure in the limb veins and those in
the thoracic region veins – drives more blood from the limbs = respiratory pump

21-56
3. skeletal muscle activity –
contraction of skeletal muscles
can push on the vein walls,
decreasing their size and
decreasing their capacity
4. venous valves – venous
vasoconstriction and skeletal
muscle contraction also drive
blood away from the heart
-evolved extensions off the endothelium –
valves
-these valves can shut off sections of veins
to prevent back-flow towards the feet
when standing

21-57
 Veins and gravity
- gravity – when lying down, forces of gravity are equally
applied to all veins
-when standing, vessels below the heart become more subject to
gravitational forces
-so the veins increase their volume to counteract the increased
volume
-this reduces the amount of blood returning to the heart –
decreases CO
-also increases the pressure in the capillaries – forces more fluid
out into the tissues from the blood
-compensatory mechanisms – fall in MAP triggers the
sympathetic NS to induce venous constriction to drive some
of the pooled blood up toward the heart + skeletal muscle
tone will increase to help propel blood to the heart

21-58
21-59