Blood Vessels

• Blood Pressure
– Review of Blood Vessels
– Blood Flow & Blood Pressure
• Arteries
• Arterioles
• Capillaries
• Veins
– Summary of Regulation
 The Cardiovascular System
• Heart: a double sided pump that establishes blood pressure,
needed to get blood flow out to the tissues.
• Blood Vessels: passageways for blood to be distributed
throughout the body and exchange materials to/from the
tissues
• Blood: liquid connective tissue that transports dissolved and
suspended materials.
 Sufficient Circulation?
• The heart needs to pump
adequately to get enough
blood to the blood vessels PULMONARY
CIRCULATION
– cardiac output

• The blood vessels receive

and respond to changes in
pressure to adequately
get blood to and from the
SYSTEMIC
tissues CIRCULATION
– blood flow
– blood pressure
 Blood Vessels
• Blood Vessels: responsible for transportation of blood from the
heart to the tissues, and from the tissues back to the heart.
• Arteries: move AWAY from the heart, toward tissues
– Arterioles
• Capillaries: microscopic blood vessels that exchange materials with
the tissues
• Veins: move TOWARD the heart, returning blood from tissues
– Venules
Systemic circulation
SYSTEMIC
CIRCULATION
(HEART) Left ventricle to:
Aorta
(major
Arteries systemic
Systemic
veins artery)
Arterioles

Capillaries (TISSUES)
Systemic
Venules Tissues capillaries

Veins Venules Arterioles

(HEART) To Right atrium

Fig. 10-4, p. 349

 Arteries
• Arteries: move AWAY from the
Endothelium
heart, toward tissues
Elastin
– Thick, elastic walls, large radius fibers
– High pressure, nearest heart when Smooth
muscle
blood is pumped out
– Expand like balloons to absorb and Elastin
store pressure of pumped blood fibers
leaving heart Connective
tisssue coat
• Collagen: tensile strength‫لشد‬66‫ا‬ ‫وة‬66‫ق‬ (mostly
collagen
• Elastin: stretch capability ‫لتمدد‬66‫علىا‬ ‫لقدرة‬66‫ا‬ fibers)

• Artery Pressure fluctuates with

systolic and diastolic events in the Endothelium
Elastin fibers
heart Smooth muscle
Collagen fibers
 Arterioles
• Arterioles: small arteries
Endothelium
– Highly muscular, dense SNS nervous system
innervation, small radius
– High resistance, slow down the flow of blood Smooth
from the arteries to decrease pressure and muscle
regulate blood flow to the tissues
• Arteriole smooth muscle contracts,
Connective
diameter can be reduced/increased to tisssue coat
(mostly
regulate blood flow collagen
• Thick, circular smooth muscle layer fibers)

Endothelium
NO Elastin fibers
Smooth muscle
Collagen fibers
Arterioles: Vasomotor
Response
• Vasoconstriction: contract smooth
muscle in arterioles to decrease
diameter of vessel
• Vasodilation: relax smooth muscle in
arterioles to increase diameter of vessel

• The vasomotor response can be

triggered in any vessel smooth muscle,
but it has the greatest effect on
arterioles.
 Capillaries
• Capillaries: microscopic blood vessels that
are the sites of exchange with tissue cells
– 50000 miles of capillaries Endothelium
– Muscle and glands highest where subcutaneous
tissue and cartilage the less
– Thin walled, less than 0.1mm from capillary
– Low blood pressure to allow slow blood flow
– Exchange occurs via diffusion
• Endothelium layer only (one cell thick)

• Permeability varies by how tight the

endothelial cells are joined together:
– Fenestrated Capillaries Endothelium
NO Elastin fibers
– Continuous Capillaries NO Smooth muscle
– Sinusiod Capillaries NO Collagen fibers
 Veins & Venules
• Veins: vessels returning blood from the
Venous
capillaries/tissues back toward the heart valve
– Thin walls, large radius, SNS nervous system Endothelium
innervation, valves, Smooth
– Easily stretched to retain blood, but NOT muscle;
elastin
elastic (do not recoil) fibers

– Slow blood flow, low pressure

Connective
• Blood reservoir: veins contain >60% of tisssue coat
(mostly
total blood volume at any given time collagen
fibers)
• Venules: small veins leaving the
capillaries
Endothelium
– Thin walls, small radius Elastin fibers
Smooth muscle
Collagen fibers
 Pulmonary Systemic
vessels arteries Systemic
9% 13% arterioles
2%
Heart
7%
Systemic
capillaries
5%

Systemic
veins
64%

Fig. 10-27, p. 371

 Blood Vessel Walls

Endothelium Venous
valve
Elastin
fibers Endothelium

Smooth Smooth
muscle muscle;
elastin
fibers
Elastin
fibers
Connective
Connective
tisssue coat
tisssue coat
(mostly
(mostly
collagen
collagen
Capillary fibers)
Large artery fibers) Arteriole Large vein
Relative Thickness
of Layers in Wall

Endothelium
Elastin fibers
Smooth muscle
Collagen fibers

Table 10-1, p. 348

Avastin (DRUG): VEGF inhibitor
Generic name: bevacizumab
 Lymphatic Vessels
• Lymphatic Vessels: vessels that
pick up excess fluid from the
capillary beds and return it to the
venous system
• Low pressure, one-way valves
formed by overlapping
endothelial cells
• Permeable to large proteins and
particles
Lymphatic
• Fluid cleaned, filtered, immune vessel
system checked at lymph nodes,
spleen
Excess fluid, protiens, particles from the tissue
Results from 11mm Hg – 9mm Hg will pick up
by Lymphatic Vessel
 Lymphatic system (LS)
• 20 liters reach capillaries --- through pores leak to ISF ---17 L reabsorbed --
• 3 liters remain will absorbed by L.S capillaries through mini-valves

Absorb Chylomicrons
Composition of Blood

19-20
Review
 Blood Vessel Measurements
• Blood vessel properties ultimately affect the delivery of
blood to the tissues and back to the heart
• Important measurements to determine adequate
function of blood vessels:
– Flow Rate: volume of blood passing through a vessel per minute
– Resistance: opposition to flow of blood through a vessel caused
by friction of blood moving inside a vessel
– Flow Velocity: speed of blood flowing through vessels
– Blood Pressure: force of blood pushing against the vessel walls
 Arteries are Pressure Reservoirs
• Arteries are elastic, allowing them to transfer pressure
from the pumping of the heart to the circulation
• Due to elastic properties of large arteries, stretch to
receive blood from ventricles, recoil to push blood out to
circulation
• Pressure changes reflect cardiac cycle changes:
– Maximum pressure= systolic pressure
• occurs when ventricles pump blood out to arteries
– Minimum pressure = diastolic pressure
• occurs when ventricles relax

• Low Resistance, due to large radius and elasticity allows

blood to flow freely without opposition
 Arteries

Arterioles

From veins To capillaries

(a) Heart contracting and emptying – systolic pressure changes, cause

arteries to expand

Arteries

Arterioles

From veins To capillaries

(b) Heart relaxing and filling – diastolic pressure changes cause

arteries to recoil
Fig. 10-6, p. 350
Blood pressure in artries and veins
Hydrostatic pressure
Velocity
 Systemic Blood Pressure
• Systemic Blood Pressure is measured at the arteries due to
their elastic properties
• How strong is the movement of blood through the circulatory
system?
– Blood Pressure: the force exerted by the blood against a vessel wall,
depends on volume of blood and stretch of vessels wall
(compliance/distensibility)
– Mean Arterial Pressure: pressure in the arteries determines the overall
pressure in the system, determined by systolic and diastolic events in
the heart
– Sphygmomanometer: a blood pressure cuff device used to measure
changes in arterial pressure
 Systolic pressure
120
110 Mean pressure
100
90
Pressure (mm Hg)

80
Diastolic
70 pressure
60
50
40
30
20
10
0
Left Large Arterioles Capillaries Venules and veins
ventricle arteries
Fig. 10-9, p. 352
 Measuring Blood Pressure
• Blood Pressure is measured at the arteries, where elastic
properties of arteries allow reflection of systolic and
diastolic pressure changes in the heart.
– Systolic Pressure: highest pressure during ventricular
contraction
– Diastolic Pressure: lowest pressure during ventricular
relaxation
– Mean Arterial Pressure: average pressure in the
system, reflects average pressure for delivery to the
tissues
– Pulse Pressure: difference between systolic and
diastolic pressure, reflects flow rate due to ΔP
 Pressure-
recording
device
Inflatable
cuff
Stethoscope

(a) Use of a sphygmomanometer in determining blood pressure Fig. 10-8, p. 351

 When blood pressure is 120/80:
When cuff pressure is greater than
120 mm Hg and exceeds blood
pressure throughout the cardiac cycle:
No blood flows through the vessel.
1 No sound is heard because no blood
is flowing.

When cuff pressure is between

120 and 80 mm Hg:
Blood flow through the vessel is turbulent whenever
blood pressure exceeds cuff pressure.
22 The first sound is heard at peak systolic pressure.

33 Intermittent sounds are produced

by turbulent spurts of flow as blood
pressure cyclically exceeds cuff pressure.

When cuff pressure is less than 80 mm Hg and is below

blood pressure throughout the cardiac cycle:
Blood flows through the vessel in
smooth, laminar fashion.
44 The last sound is heard at minimum
diastolic pressure.
55 No sound is heard thereafter because
of uninterrupted, smooth, laminar flow.
(b) Blood flow through the brachial artery in relation to cuff pressure and sounds Fig. 10-8, p. 351
 Blood Pressure Equations
• Mean Arterial Pressure: average pressure in the system,
reflects average pressure for delivery to the tissues, it
depends on the pressure of blood leaving the heart and
entering the blood vessels

[MAP = diastolic BP + 1/3(systolic – diastolic)]

or:
[MAP = CO x TPR]

–systolic & diastolic pressures are measured

–CO = cardiac output (amount of blood pumped in one minute)
–TPR = total peripheral resistance (opposition to blood flow that
keeps blood in the arteries)
MAP depends on CO, BLOOD volume, resistence (diameter of arteriols) and distribution of blood betw art and veins
(this depend on diameter of veins)
Mean Arterial Pressure (MAP)
 Blood Flow
• How much blood flows through a vessel at any given time?
The rate of blood flow is affected by the pressure in the vessel
and the resistance in the vessel
– Flow Rate: volume of blood passing through a vessel per
minute
• Flow Rate Depends on:
• Pressure gradient
• Vessel Resistance
 Blood Flow
• Blood Flow:
– Pressure gradient: difference in pressure from
beginning to end of vessel
• Blood flows from high to low pressure
• determined by cardiac output, vessel stretch/compliance
– Resistance: opposition to flow of blood through a
vessel caused by friction of blood moving inside a
vessel
• blood flow decreases when resistance increases
• Viscosity: blood thickness, number of red blood cells
increases resistance
• Blood vessel length: longer vessels increase resistance
• Blood vessel radius: smaller diameter increases resistance
 Blood Flow Equations
[Flow Rate = ΔP/R]
ΔP = change in pressure
R = resistance
•Flow rate is increased by the change in pressure and decreased
by resistance

[Resistance = R=ηL/r4]
η = viscosity
L = length
r= radius
•Resistance is increased by viscosity, length, but decreased by
radius
•Radius is 4-fold stronger effect than viscosity and length
Flow rate = ΔP/R
Flow rate decreases when R increases

Example: if the ΔP is the same, a vessel with high

resistance, or small radius, will have decreased flow rate

10 ml

10
ml

radius of vessel1 = 1mm

radius of vessel2 = 2mm
Resistance vessel2 = 1/16
Flow in vessel2 = 16 times higher than in vessel1 Fig. 10-3, p. 346
 50 mm Hg 10 mm Hg
Flow rate = ΔP/R pressure pressure

Flow rate ∆P = 40 mm Hg
increases when Vessel 1
∆P increases 90 mm Hg 10 mm Hg
pressure pressure
Example: if the
resistance is the ∆P = 80 mm Hg
Vessel 2
same, a vessel
with higher ΔP will
have
∆P in vessel 1 = 40 mmHg
proportionally
higher Flow rate ∆P in vessel 2 = 80 mmHg

Flow in vessel 2 = 2 times that of

vessel 1

Fig. 10-2, p. 345

 90 mm Hg 10 mm Hg
Flow rate = ΔP/R pressure pressure

Flow rate is the ∆P = 80 mm Hg

Vessel 2
same if ΔP and R
are equivalent 180 mm Hg 100 mm Hg
pressure pressure

Example: if the ∆P = 80 mm Hg
resistance is the Vessel 3
same, and ΔP is
equivalent, then the
flow rate will not ∆P in vessel 2 = 80 mmHG
change, even if the ∆P in vessel 3 = 80 mmHG

Pressure values Flow in vessel 3 = the same as that

start at very different of vessel 2
levels

Fig. 10-2, p. 345

R=ηL/r4

Radius effects on resistance and blood flow are 4-fold

changes

Vessel 1

Same
pressure
gradient

Vessel 2

Radius in vessel 2 = 2 times that of vessel 1

Resistance in vessel 2 = 1/16 that of vessel 1
Flow in vessel 2 = 16 times higher than that of vessel 1

Fig. 10-3, p. 346

 Arterioles have High Resistance
• Arterioles have high resistance and are the major
determinants of flow rate in the body
• DO NOT expand/recoil like the arteries, flow rate is
determined by mainly by resistance
– small radius vessels
– adjustable radius via vasoconstriction, vasodilation of
smooth muscle in arteriole walls
 Constant pressure in pipe
(mean arterial pressure)
From pump
(heart)

High Moderate Low

resistance resistance resistance

No flow Moderate flow Large flow

KEY
Control valves = Arterioles

Fig. 10-11, p. 354

 Control of Arteriole radius
Many ways to cause changes in arterioles:
– Local Control: changes within an organ to increase or
decrease supply of blood to that organ
• Metabolic (via paracrine signals)
• Histamine
• Stretch
• Shear stress
• Temperature
– Extrinsic Control: changes to the entire system of
blood vessels to increase or decrease blood flow and
blood pressure in the body
• SNS; norepinephrine
• Hormones; epinephrine, norepinephrine, vasopressin,
angiotensin II
 Local Control: Metabolic
• Metabolic changes match organ
needs with local blood flow
– Vasodilation to increase blood flow to the
tissues will be triggered when tissues are
more metabolically active:
• Decreased O2, increased CO2,
increased acid (H+ or lactic acid),
increased K+, increased osmolarity,
increased adenosine
– Vasoconstriction to decrease blood flow
to less active tissues
• opposite effects
Vasodilation in more
• Most pronounced in heart, skeletal metabolically active
muscle, brain tissues
• Can alter the overall distribution of
cardiac output to various organs
 Endothelial Paracrine Release
• Metabolic chemical changes act indirectly on
blood vessels by causing paracrine release
• Endothelial cells in all blood vessels release
paracrines in response to metabolic changes
• Most studied is Nitric Oxide:
– causes vasodilation; relaxation of smooth
muscle via g-protein coupled receptor
mechanism and phosphorylation of
myosin
• Others include:
– Endothelin
• Causes vasoconstriction Vasodilation in more
– VEGF (vascular endothelial growth factor) metabolically active
tissues
• Causes new vessel growth
– Histamine
• Inflamation- vasodilation- Incr blood flow- WBC
to the area
 Extrinsic Control: Hormones
• Hormones released from the
adrenal medulla, epinephrine,
norepinephrine, reinforce SNS
activity and cause vasoconstriction
• Other hormones:
• Vasopressin (ADH)
– vasoconstriction
– retains water, increases blood volume
• Angiotensin II
Vasoconstriction in
– Vasoconstriction response to
– Retains Na+ and water, increases blood hormones
volume
 Vasoconstriction

Caused by:
Myogenic activity
Oxygen (O2)
Carbon dioxide (CO2)
And other metabolites
Endothelin
Sympathetic stimulation
Vasopression; angiotensin II
Cold

(c) Vasoconstriction (increased contraction of circular

smooth muscle in the arteriolar wall, which leads to
increased resistance and decreased flow through the vessel)

Fig. 10-10, p. 353

 Vasodilation

Caused by:
Myogenic activity
O2
CO2 and other metabolites
Nitric oxide
Sympathetic stimulation
Histamine release
Cold

(d) Vasodilation (decreased contraction of circular smooth

muscle in the arteriolar wall, which leads to decreased
resistance and increased flow through the vessel)

Fig. 10-10, p. 353

 Total peripheral
resistance
Summary of
Effects on Arteriolar
radius
Blood
viscosity

Arteriole
Number of
radius red blood
cells

Local (intrinsic) control Extrinsic control

Heat, cold application (local changes acting on (important in
arteriolar smooth muscle regulation of blood
(therapeutic use) in the vicinity) pressure)

Response to shear stress Vasopressin

(compensates for (hormone important
changes in longitudinal in fluid balance; exerts
force of blood flow) vasoconstrictor effect)

Myogenic responses to Angiotensin II

stretch (important in (hormone important
autoregulation) in fluid balance; exerts
vasoconstrictor effect)

Epinephrine and nor-

Histamine release epinephrine (hormones that
(involved with injuries generally reinforce
and allergic responses) sympathetic nervous
system)
Local metabolic changes Sympathetic activity
In O2 and other (exerts generalized
Metabolites (important in
matching blood flow with
vasoconstrictor effect)
metabolic needs)

Major factors affecting arteriolar radius Fig. 10-14, p. 360

 Capillary Exchange
• Arteriole regulation of resistance ensures adequate delivery to
the tissues
• Once the blood reaches the tissues, exchange occurs at the
capillaries
• This occurs via movement of materials into the interstitial fluid

Capillaries  interstitial fluid  cells

• Diffusion: solutes move along their concentration gradients

• Bulk Flow: water and solutes flow together through capillary
pores, proteins stay inside
 Capillaries
• Precapillary sphincters can control the flow of blood through
the capillary beds
– Smooth muscle that respond to local controls
 Blood Pressure Equations
• Blood Pressure is regulated by cardiac output and
arteriole resistance, total peripheral resistance
MAP = CO * TPR

– Cardiac output (CO) is regulated by stroke volume and

heart rate
CO = SV * HR

– Total Peripheral Resistance (TPR) is regulated by

arteriole radius and blood viscosity

R = ηL/r4
 Regulating Blood Pressure
MAP = CO * TPR

•In other words, systemic blood pressure will increase with:

– Cardiac output increases:
• Increased stroke volume (heart contractility, venous return)
• Increased heart rate (intrinsic conduction)
– Resistance increases
• Increased vasoconstriction (arteriole radius)
• Increased blood viscosity (RBC production)
 Baroreceptor Reflexes
Carotid sinus
• Baroreceptors are pressure baroreceptor
receptors in the aortic arch and
Aortic arch
carotid arteries
baroreceptor
• Action potentials are sent from the
baroreceptors to the Medulla
cardiovascular control centers
• If too low, SNS will increase blood
pressure:
– Increase heart rate and
contractility (increase CO)
– Increase vasoconstriction (TPR) to
increase systemic blood pressure
• If too high: PSNS will decrease
blood pressure:
– decrease heart rate (decrease CO)
 Normal Increased Decreased

Arterial
120
pressure
(mm Hg)

80 Mean
pressure

Firing rate in
afferent neuron
arising from carotid
sinus baroreceptor

Time

Fig. 10-36, p. 378

 Baroreceptor Reflex: SNS effects

When blood pressure Carotid sinus Rate of firing Cardiovascular

falls below normal and aortic arch center
in afferent nerves
receptor potential

Sympathetic cardiac nerve activity Heart rate Blood

and Cardiac output
and pressure
stroke volume and
sympathetic vasoconstrictor nerve activity increased
and total peripheral
and toward
parasympathetic nerve activity arteriolar and resistance
normal
venous vasoconstriction

(b) Baroreceptor reflex in response to a fall in blood pressure

Stepped Art
Fig. 10-38, p. 379
 Autonomic Effects on Blood Pressure

Parasympathetic Heart Cardiac Blood

stimulation Heart rate output pressure

Heart
rate
Sympathetic Cardiac Blood
stimulation Heart output pressure
Contractile Stroke
strength volume
of heart

Total peripheral Blood

Arterioles Vasoconstriction
resistance pressure

Venous Stroke Cardiac Blood

Veins Vasoconstriction
return volume output pressure

Fig. 10-37, p. 378

 Cardiovascular Center in
Medulla Oblongata
Control Center for heart and blood vessels

Cardiovascular center –cardiac centers plus the vasomotor

center that integrate blood pressure control by altering cardiac
output and blood vessel diameter

A. Cardio center
Autonomic of the heart
- Cardioaccelatory center: sympathetic
- Cardioinhibitory center: Parasympathatic
B. Vasomotor center
Autonomic control of the heart
-Stimulation of vasomotor center: Vasoconstriction (Sympathatic)
- Inhibition of vasomotor center: Vasodilation
 Cardio-vascular regulation
• Middle Group of Neurons (MGN)
(hypothalamus)

Cardio-inhibitory centres (CIC)

(Medulla Oblongata)

Connected to Parasympathetic nerve through

Efferent Vagus (release of Ach neurotransmitter)

Muscarinic receptors on SA node

Stimulation = HR & BP
 Posterior Group of Neurons (PGN)
(hypothalamus)

Cardio-acceleratory centres (CEC)

(Medulla Oblongata)

Connected to Sympathetic nerve through

cardiac plexus (release of adrenaline
neurotransmitter)
Beta receptors on SA node

Stimulation = HR & BP
Control of the Vasomotor Center by Higher Nervous
Centers.
Hypothalamus:
- Is higher integrated center of autonomic system, including
feeding, regulation of body temperature, fluid balance and
endocrine secretion.
- It has a powerful excitatory or inhibitory effects on the
vasomotor center.
- The posterolateral portions of the hypothalamus cause mainly
excitation, so increases HR & BP
- The anterior portion can cause either mild excitation or
inhibition, depending on the precise part of the anterior
hypothalamus stimulated.
Control of the Vasomotor Center by Higher
Nervous Centers.
Cerebral cortex
By affecting hypothalamus then VMC
- Many parts of the cerebral cortex can also excite or inhibit
the vasomotor center.
(1) Limbic area regulates the activity of lower centers.
(2) motor and premotor causes vasoconstriction of skin
and renal vessels but vasodilation of skeletal muscle
(3) Responses of BP to pain, anxiety and during exercise.
Short-Term Mechanisms: Baroreceptor-Initiated
Reflexes
• Increased blood pressure stimulates the cardioinhibitory center to:
• Increase vessel diameter
• Decrease heart rate, cardiac output, peripheral resistance, and blood pressure

• Declining blood pressure stimulates the cardioacceleratory center to:

• Increase cardiac output and peripheral resistance
• Low blood pressure also stimulates the vasomotor center to constrict
blood vessels
Reflex : very fast
and short term
 Impulse traveling along
afferent nerves from
baroreceptors:
Stimulate cardio-
inhibitory center Sympathetic
(and inhibit cardio-
acceleratory center)
impulses to
heart Cardio
( HR and contractility)

Baroreceptors
in carotid
sinuses and
aortic arch Inhibit CO
stimulated vasomotor center
R

Rate of vasomotor
Arterial
blood pressure
Vaso impulses allows
vasodilation CO and R
rises above ( vessel diameter)
normal range
return blood
pressure to
Stimulus: homeostatic
Rising blood range
pressure

Homeostasis: Blood pressure in normal range

Figure 19.8
 Homeostasis: Blood pressure in normal range
Stimulus:
Declining
blood pressure

CO and R
return blood Impulses from
pressure to baroreceptors: Arterial blood pressure
homeostatic Stimulate cardio- falls below normal range
range acceleratory center
Cardiac (and inhibit cardio-
output inhibitory center) Baroreceptors in
(CO) carotid sinuses
Sympathetic and aortic arch
impulses to heart inhibited
Peripheral ( HR and contractility)
resistance (R)

Vasomotor Stimulate
Fibers vasomotor
stimulate center
vasoconstriction

Figure 19.8
Glossopharyngeal
 Control of Arterial Pressure by the Carotid
and Aortic Chemoreceptor
• The chemoreceptors are cells sensitive to O2 lack, CO2 and H+ excess.
• They are located in the two carotid bodies, and several aortic bodies adjacent to
the aorta.
• chemoreceptors are always in close contact with arterial blood.
• The chemoreceptors excite nerve fibres that, along with the baroreceptor fibres,
pass through the vagus nerve into the vasomotor centre
• Whenever the arterial pressure falls below a critical level (below 80 mm Hg), the
chemoreceptors become stimulated (due to lack O2, or excess CO2)
• The signals transmitted from the chemoreceptors excite the vasomotor center,
and this elevates the arterial pressure back toward normal.
• This reflex becomes specially important in critical hypotension to help prevent
still further fall in pressure.
 • Low blood O2, high CO2, low pH  stimulate VMC
decrease parasympathetic
Increase sympathetic
Vasoconstriction
Increase HR, SV

 Increase in BP (speeding the return of blood to the heart and

lung)
Chemicals that Increase Blood Pressure

• Adrenal medulla hormones – norepinephrine and epinephrine

increase blood pressure
• Antidiuretic hormone (ADH) – causes intense vasoconstriction in
cases of extremely low BP-prevent loss of water in urine (water
reabsorption)—produced by hypothalamus
• Angiotensin II – kidney release of renin generates angiotensin II,
which causes vasoconstriction
• Endothelium-derived factors – endothelin and prostaglandin-derived
growth factor (PDGF) are both vasoconstrictors
Chemicals that Decrease Blood Pressure

• Atrial natriuretic peptide (ANP) – causes blood volume and pressure

to decline– released by cells in right atria in response to high BP and
blood volume---- cause vasodilation and increase loss of Na in urine
• Nitric oxide (NO) – is a brief but potent vasodilator
• Inflammatory chemicals – histamine, prostacyclin, and kinins are
potent vasodilators
• Alcohol – causes BP to drop by inhibiting ADH
• Bradykinin: powerfull arterior dilation deactivated by same ACE.
• Histamine: release in response to damage and inflammation, most
derived from mast cell. Powerfull arterioles vasodilators and
pearmebility
Kidney Action and Blood Pressure

• Declining BP causes the release of

renin, which triggers the release
of angiotensin II
• Angiotensin II is a potent
vasoconstrictor that stimulates
aldosterone secretion
• Aldosterone enhances renal
reabsorption and stimulates ADH
release
 Renin-angiotensin mechanism for arterial
pressure control
• Angiotensin causes the kidneys to retain both salt and
water in two major ways:
1. It acts directly on the kidneys to cause salt and water
retention.
2. It causes the adrenal glands to secrete aldosterone, which
increases salt and water reabsorption by the kidney tubules.

• This angiotensin effect has a long-term effect, and is

more powerful than the acute vasoconstrictor
mechanism in raising the arterial pressure.
 Cardiovascular Disease
• Cardiovascular disease accounts for over
half of all deaths in the United States
• Myocardial infarction - heart attack
Aorta
• When heart muscle
does not receive blood, Coronary artery
cells will quickly die
• Cause by blockage of
coronary arteries Blockage

Dead
muscle
tissue

Figure 23.14
 Cardiovascular Disease
• Atherosclerosis
• Narrowing of the arteries by plaques of cholesterol
and other substances that form in the inner walls of
arteries

Figure 23.15
Atherosclerosis