W.

O CARDIO WEEK 2 dari optimal length (lo) dimana lo ini

2. a. Describe mechanism of cardiac
reserve
 Heart rate
 Stroke volume, venous return
 Central venous pressure
 Cardiac output
 Blood flow and regulation
 Myocardial consumption
adalah max tension yg didevelop pas
kontraksi. Makanya length cardiac muscle
fiber varies along ascending limb of
length-tension curve. Pemanjangan di
cardiac muscle fiber length dengan
mendekat ke lo ini bakalan bkin kenaikan
contractile tension of heart following
sistol.

Cardiac output (CO) itu kan volume darah Preload: degree of stretch of cardiac
yang dipompa sama tiap ventrikel per muscle cells before they contract (Frank-
menit. Starling law of the heart)
BP = CO x TPR Closely related to LV end-diastolic volume
CO sendiri depends on: CO = SV x HR, Cardiac muscle exhibits a length-tension
dimana SV(EDV-ESV) depends on 3: relationship
 Cardiac contractility At rest, cardiac muscle cells are shorter
 Venous return to heart (preload) than optimal length
Slow heartbeat and exercise increase
 Resistance the LV must overcome
venous return
to eject blood into aorta
Increased venous return distends
(afterload)
(stretches) the ventricles and increases
Stroke volume di determined by the
contraction force
extent of venous return and by
Contractility: contractile strength at a
sympathetic activity. The other
given muscle length, independent of
component besides heart rate that
muscle stretch and EDV
determines cardiac output is stroke
• A Fundamental property of cardiac
volume.
muscle reflects the level of
Ada 2 types of controls yg influence stroke
activation of cross-bridge
volume:
formation
(1) intrinsic control related to the extent
• Positive inotropic agents increase
of venous return
contractility
(2) extrinsic control related to the extent
– Increased Ca2+ influx due to
of sympathetic stimulation of the heart.
sympathetic stimulation
Dua2ny bakalan naikkin SV dgn naikkin
– Hormones (thyroxine,
strength dari heart contraction.
glucagon, and epinephrine)
• Negative inotropic agents decrease
Penaikkan EDV bakalan bkin penaikkan
contractility
SV. Intrinsic control of SV yg refer ke
– Acidosis
hearts inherent ability buat vary SV,
– Increased extracellular K+
depend sama direct correlation antara
– Calcium channel blockers
EDV dan SV. Semakin banyak darah balik
Afterload: pressure that must be
ke jantung, jantung bakalan pompa lebih
overcome for ventricles to eject blood
byk darah tp jantung ga eject smua
• closely related to aortic impedance
darahny.Disini intrinsic control
(i.e., the sum of the external
bergantung sama length-tension
factors that oppose ventricular
relationship dari cardiac muscle. Resting
ejection);
cardiac muscle fiber length nya kurang
 • Hypertension increases afterload,
resulting in increased ESV and
reduced SV
End Diastolic Volume (EDV)
 Workload on the heart prior to
contraction (preload).
 Volume of blood in the ventricles
at the end of diastole.is about 130
mL.
 SV directly proportional to
preload.
 Increase in EDV results in an
increase in SV.
 SV directly proportional to
contractility.
 Strength of contraction varies
directly with EDV.
 Ejection fraction: - SV/ EDV.
- Normally is 60%.
- Clinical diagnostic tool.
End-systolic ventricular volume, (ESV)
 The ventricle does not empty
completely during ejection
 blood remains in each ventricle at
the end of systole when ejection is
complete is about 50 mL
Cardiac reserve: perbedaan CO pas lagi
istirahat sama pas lagi maximumnya (cth
pas olahraga CO semakin tinggi)
Heart rate sendiri didetermined sama
autonomic influence di SA node. SA node
biasanya pacemaker jantung karena dia yg
fastest spontaneous rate of depolarization
to threshold. Trus automatic gradual
reduction of membrane potential
between beats nya itu hasil produk dari
complex interplay of ion movements
involving an increase in Na permeability, a
reduction in K permeability, and an
increase in Ca2 permeability. Pas SA node
reaches threshold, an action potential is
initiated menjalar ke seluruh jantung,
inducing the heart to contract, or have a
“heartbeat.”
The heart is innervated by both divisions
of the autonomic nervous system, which
can modify the rate (as well as the
strength) of contraction, even though
nervous stimulation is not required to
initiate contraction. Th e parasympathetic
nerve to the heart, the vagus nerve,
primarily supplies the atrium, especially
the SA and AV nodes. Parasympathetic
innervation of the ventricles is sparse. The
cardiac sympathetic nerves also supply
the atria, including the SA and AV nodes,
and richly innervate the ventricles as well.
Although autonomic innervation is the
primary means by which heart rate is
regulated, other factors kayak
epinephrine disecreted into the blood
from the adrenal medulla on sympathetic
stimulation. Epinephrine increase heart
rate, thus reinforcing the direct effect that
the sympathetic nervous system has on
the heart.
FRANK–STARLING LAW OF THE HEART too much blood would be dammed up in
Apa yang bikin cardiac muscle fibers to the venous system before the ventricle
vary in length before contraction? Skeletal with the lower output.
muscle length bisa vary before contraction 2. when a larger cardiac output is needed,
because of the positioning of the skeletal such as during exercise, venous return is
parts to which the muscle is attached, but increased through action of the
cardiac muscle is not attached to any sympathetic nervous system and other
bones. The main determinant of cardiac mechanisms to be described in the next
muscle fiber length is the degree of chapter. The resulting increase in EDV
diastolic filling. An analogy is a balloon automatically increases stroke volume
filled with water—the more water you put correspondingly. Because exercise also
in, the larger the balloon becomes, and increases heart rate, these two factors act
the more it is stretched. Likewise, the together to increase the cardiac output so
greater the diastolic filling, the larger the that more blood can be delivered to the
end-diastolic volume (EDV), and the more exercising muscles.
the heart is stretched. The more the heart
is stretched, the longer the initial cardiac
fiber length before contraction. The
increased length results in a greater force
on the subsequent cardiac contraction
and thus in a greater stroke volume. Th is
intrinsic relationship between EDV and
stroke volume is known as the Frank–
Starling law of the heart.
Stated simply, the law says that the heart
normally pumps out during systole the
volume of blood returned to it during
diastole; increased venous return results
in increased stroke volume.
Jadi buat maintain homeostasis,
reconditioning organs bakalan terima
ADVANTAGES OF THE CARDIAC LENGTH–
blood flow in excess of their own needs.
TENSION RELATIONSHIP
Blood is constantly “reconditioned” so
1. Dia bikin equal output between the
that its composition remains relatively
right and left sides of the heart so that
constant despite an ongoing drain of
blood pumped out by the heart is equally
supplies to support metabolic activities
distributed between the pulmonary and
and despite the continual addition of
systemic circulation. If, for example, the
wastes from the tissues.
right side of the heart ejects a larger
Organs that recondition the blood
stroke volume, more blood enters the
normally receive much more blood than is
pulmonary circulation, so venous return
necessary to meet their basic metabolic
to the left side of the heart increases
needs, so they can adjust the extra blood
accordingly. The increased EDV of the left
to achieve homeostasis.
side of the heart causes it to contract
For example, large percentages of the
more forcefully, so it too pumps out a
cardiac output are distributed to the
larger stroke volume. In this way, output
digestive tract (to pick up nutrient
of the two ventricular chambers is kept
supplies), to the kidneys (to eliminate
equal. If such equalization did not happen,
metabolic wastes and adjust water and
electrolyte composition), and to the skin
(to eliminate heat). Blood flow to the
other organs—heart, skeletal muscles,
and so on—is solely for filling these
organs’ metabolic needs and can be
adjusted according to their level of
activity. For example, during exercise
additional blood is delivered to the active
muscles to meet their increased metabolic
needs. Because reconditioning organs—
digestive organs, kidneys, and skin—
receive blood flow in excess of their own
needs, they can withstand temporary
reductions in blood flow much better than
other organs can that do not have this
extra margin of blood supply. The brain in
particular suffers irreparable damage
when transiently deprived of blood
supply. After only four minutes without
O2, permanent brain damage occurs.
Therefore, constant delivery of adequate
blood to the brain, which can least
tolerate disrupted blood supply, is a high
priority in the overall operation of the
circulatory system. In contrast, the
reconditioning organs can tolerate
significant reductions in blood flow for
quite a long time, and often do. For
example, during exercise some of the
blood that normally flows through the
digestive organs and kidneys is diverted to
the skeletal muscles. Likewise, to
conserve body heat, blood flow through
the skin is markedly restricted during
exposure to cold.
Blood flow through a vessel depends on
the pressure gradient and vascular
resistance. The flow rate of blood through
a vessel is directly proportional to the
pressure gradient and inversely
proportional to vascular resistance:
PRESSURE GRADIENT
The pressure gradient is the difference in
pressure between the beginning and end
of a vessel. Blood flows from an area of
higher pressure to an area of lower
pressure down a pressure gradient.
Contraction of the heart imparts pressure
to the blood, which is the main driving
force for flow through a vessel. Because of
frictional losses (resistance), the pressure
drops as blood flows throughout the
vessel’s length. Accordingly, pressure is
higher at the beginning than at the end of
the vessel, establishing a pressure
gradient for forward flow of blood
through the vessel. The greater the
pressure gradient forcing blood through a
vessel, the greater the flow rate is through
that vessel. Think of a garden hose
attached to a faucet. If you turn on the
faucet slightly, a small stream of water
will flow out of the end of the hose,
because the pressure is slightly greater at
the beginning than at the end of the hose.
If you open the faucet all the way, the
pressure gradient increases tremendously,
so that water flows through the hose
much faster and spurts from the end of
the hose. Note that the difference in
pressure between the two ends of a
vessel, not the absolute pressures within
the vessel, determines flow rate
RESISTANCE
The other factor influencing flow rate
through a vessel is resistance, which is a
measure of the hindrance or opposition to
blood flow through the vessel, caused by
friction between the moving fluid and the
stationary vascular walls. As resistance to control of vascular resistance. Therefore,
flow increases, it is more difficult for the major determinant of resistance to
blood to pass through the vessel, so flow flow is the vessel’s radius. Fluid passes
rate decreases (as long as the pressure more readily through a large vessel than
gradient remains unchanged). When through a smaller vessel.
resistance increases, the pressure The reason is that a given volume of blood
gradient must increase correspondingly to comes into contact with much more of
maintain the same flow rate. Accordingly, the surface area of a small-radius vessel
when the vessels offer more resistance to than of a larger-radius vessel, resulting in
flow, the heart must work harder to greater resistance
maintain adequate circulation. Furthermore, a slight change in the radius
Resistance to blood flow depends on of a vessel brings about a notable change
three factors: in flow, because the resistance is inversely
(1) viscosity of the blood, proportional to the fourth power of the
(2) vessel length, radius (multiplying the radius by itself four
(3) vessel radius, which is by far the most times):
important. The term viscosity (designated
as ,) refers to the friction developed
between the molecules of a fluid as they
slide over each other during flow of the
fluid. The greater the viscosity, the greater
the resistance to flow is. In general, the
thicker a liquid, the more viscous it is. For
example, molasses flows more slowly than
water because molasses has greater
viscosity. Blood viscosity is determined
primarily by the number of circulating red
blood cells. Normally, this factor is
relatively constant and not important in
controlling resistance.
Occasionally, however, blood viscosity and
resistance to flow are altered by an
abnormal number of red blood cells.
When excessive red blood cells are
present, blood flow is more sluggish than
normal. Because blood “rubs” against the
lining of the vessels as it flows past, the
greater the vessel surface area in contact
with the blood, the greater the resistance
to flow is.
Surface area is determined by both the
length (L) and radius (r) of the vessel. At a
constant radius, the longer the vessel is,
the greater the surface area and the
greater the resistance to flow. Because
vessel length remains constant in the
body, it is not a variable factor in the

b. Describe the determinants of blood
flow as equations
BP is the product of cardiac output (CO)
and total peripheral resistance (TPR):
BP = CO x TPR
And CO is the product of cardiac stroke
volume (SV) and heart rate (HR):
CO = SV x HR
SV is determined by
(1) cardiac contractility;
(2) the venous return to the heart
(preload);
(3) the resistance the left ventricle must
overcome to eject blood into the aorta
(afterload).
d. Describe function of vascular
endothelium and smooth muscle
Vascular endothelium: a thin membrane
that lines the inside of the heart and blood
vessels. Endothelial cells release
substances that control vascular
relaxation and contraction as well as
enzymes that control blood clotting,
immune function and platelet (a colorless
substance in the blood) adhesion.
Function:
 Barrier function - the endothelium acts
as a semi-selective barrier between the
vessel lumen and surrounding tissue,
controlling the passage of materials and
the transit of white blood cells into and
out of the bloodstream. Excessive or
prolonged increases in permeability of
the endothelial monolayer, as in cases
of chronic inflammation, may lead to
tissue edema/swelling. Altered barrier
function is also implicated in cancer
extravasation.
 Blood
clotting (thrombosis & fibrinolysis). The
endothelium normally provides a non-
thrombogenic surface because it
contains, for example, heparan
sulfate which acts as a cofactor for
activating antithrombin, a protease that
inactivates several factors in the
coagulation cascade.
 Inflammation. Endothelial cells actively
signal to immune cells during
inflammation
 Formation of new blood vessels
(angiogenesis)
 Vasoconstriction and vasodilation, and
hence the control of blood pressure
 Repair of damaged or diseased organs
via an injection of blood vessel cells[9]
 Angiopoietin-2 works with VEGF to
facilitate cell proliferation and migration
of endothelial cells
Smooth Muscle
Smooth muscle is a type of muscle
tissue which is used by various systems to
apply pressure to vessels and organs.
Smooth muscle is composed of sheets or
strands of smooth muscle cells. These cells
have fibers of actin and myosin which run
through the cell and are supported by a
framework of other proteins. Smooth muscle
contracts under certain stimuli as ATP is
freed for use by the myosin. The amount of
ATP released depends on the intensity of
the stimuli, allowing smooth muscle to have
a graded contraction as opposed to the “on-
or-off” contraction of skeletal muscle.
VASOCONSTRICTION AND
VASODILATION
Unlike arteries, arteriolar walls contain very
little elastic connective tissue tapi ada thick
layer of smooth muscle that is richly
innervated by sympathetic nerve fibers. The
smooth muscle layer runs circularly around
the arteriole so when the smooth muscle
layer contracts, the vessel’s circumference
(and its radius) becomes smaller, increasing
resistance and decreasing flow through that
vessel - Vasoconstriction
Vasodilation - enlargement in the
circumference and radius of a vessel as a
result of its smooth muscle layer relaxing
Vasodilation leads to decreased resistance
and increased flow through that vessel.
VASCULAR TONE
The extent of contraction of arteriolar
smooth muscle depends on the cytosolic
concentration of Ca2. Arteriolar smooth
muscle normally displays a state of partial
constriction known as vascular tone, which
establishes a baseline of arteriolar
resistance.
Two factors are responsible for vascular
tone.
1. arteriolar smooth muscle is tonic smooth
muscle that has sufficient surface-
membrane Ca2! channels open even at
resting potential to trigger partial contraction.
This myogenic activity is independent of any
neural or hormonal influences, leading to
self-induced contractile activity
2. the sympathetic fibers supplying most
arterioles continually release
norepinephrine, which further enhances
vascular tone. This ongoing tonic activity
makes it possible to either increase or
decrease the level of contractile activity to
accomplish vasoconstriction or vasodilation,
respectively. Were it not for tone, it would be
impossible to reduce the tension in an
arteriolar wall to accomplish vasodilation;
only varying degrees of vasoconstriction
would be possible. A variety of factors can
influence the level of contractile activity in
arteriolar smooth muscle, thereby
substantially changing resistance to flow in
these vessels. Unlike skeletal and cardiac
muscle in which action potentials trigger
muscle contraction, vascular smooth muscle
can undergo graded changes in force in
response to chemical, physical, and neural
factors with little or no accompanying
change in membrane potential. These
agents largely act via second-messenger
systems, such as the IP3/Ca2! pathway The
factors that cause arteriolar vasoconstriction
or vasodilation fall into two categories: local
(intrinsic) controls, which are important in
determining the distribution of cardiac
output; and extrinsic controls, which are
important in blood pressure regulation.
Local (intrinsic) controls are changes within
an organ that alter the radius of the vessels
and hence adjust blood flow through the
organ by directly affecting the smooth
muscle of the organ’s arterioles. Local
influences may be either chemical or
physical.
Local chemical influences on arteriolar
radius include
– local metabolic changes
– histamine release.
Local physical influences include
– local application of heat or cold,
– chemical response to shear stress,
– myogenic response to stretch.
Functions of Endothelial Cells
■ Line the blood vessels and heart
chambers; serve as a physical barrier
between the blood and the remainder of the
vessel wall
■ Secrete vasoactive substances in
response to local chemical and physical
changes; these substances cause relaxation
(vasodilation) or contraction
(vasoconstriction) of the underlying smooth
muscle
■ Secrete substances that stimulate new
vessel growth and proliferation of smooth
muscle cells in vessel walls
■ Participate in the exchange of materials
between the blood and surrounding tissue
cells across capillaries through vesicular
transport
■ Influence formation of platelet plugs,
clotting, and clot dissolution
■ Participate in the determination of capillary
permeability by contracting to vary the size
of the pores between adjacent endothelial
cells
Smooth Muscle Structure
Smooth muscle tissue, unlike skeletal or
cardiac tissues, does not have clearly
defined striations visible on the cells. This is
because smooth muscle cells are organized
in a different way than other muscle cells. As
seen in the image below, the actin and
myosin filaments in smooth muscle are
arranged in a stacked pattern across the
cell. This “staircase” arrangement of actin
and myosin is much different than the
structure in skeletal and cardiac muscle. The
actin filaments (red lines) in smooth muscle
run from one side of the cell to the other,
connecting at dense bodies and at the cell
membrane. In skeletal and cardiac muscle,
the actin filaments are attached to Z plates,
which hold many actin filaments and show
up as dark bands under the microscope. In
smooth muscle, the actin and myosin fibers
are arranged an angles to each other as
they run through the cell. This can be seen
in the image below.
Function of Smooth Muscle
Like all muscle tissue, the function of
smooth muscle is to contract. The image
above shows how the actin and myosin
fibers shorten, effectively shrinking the cell.
However, there are some important
differences in how the smooth muscle
contracts, compared to other types of
muscle. In skeletal muscle, a signal from
the somatic nervous system traverses to the
muscle, where it stimulates organelles in
the muscle cell to release calcium. The
calcium causes a protein to detach from
actin, and myosin quickly binds to the
opening on actin. Since there was always
available ATP, the myosin uses it to quickly
contract the cell.
The same is not true in smooth muscle
tissue. In smooth muscle, the contraction is
not controlled voluntarily by the
somatic nervous system, but by signals from
the autonomous nervous system, such as
nerve impulses, hormones, and other
chemicals released by specialized organs.
Smooth muscle is specialized to contract
persistently, unlike skeletal muscle which
much contract and release quickly. Instead
of a calcium trigger which sets off a
contraction reaction, smooth muscle has
more of a throttle, like in a car.
A nerve impulse or outside stimulus reaches
the cell, which tells it to release calcium.
Smooth muscle cells do not have a special
protein on actin which prevents myosin from
binding. Rather, actin and myosin are
constantly binding. But, myosin can only
hold on and crawl forward when given
energy. Inside smooth muscle cells is a
complex pathway which allows the level of
calcium to control the amount of ATP
available to myosin. Thus, when the
stimulus is removed, the cells do not relax
right away. Myosin continues to bind to actin
and crawl along the filaments until the level
of calcium falls.
Smooth Muscle Location
This specialized function of contracting for
long periods and hold that force is why
smooth muscle has been adapted to many
areas of the body. Smooth muscle lines
many parts of the circulatory
system, digestive system, and is even
responsible for raising the hairs on your arm.
In the circulatory system, smooth muscle
plays a vital role in maintaining and
controlling the blood pressure and flow of
oxygen throughout the body. While the
majority of the pressure is applied by
the heart, every vein and artery is lined with
smooth muscle. These small muscles can
contract to apply pressure to the system or
relax to allow more blood to flow.
Smooth muscle also lines the majority of the
digestive system, for similar reasons.
However, the cells in the digestive system
have different stimuli than those in the
circulatory system. For instance, sheets of
smooth muscle tissue in the gut react to you
swallowing. When you swallow, tension is
applied to one side of the sheet. The cells
on that side contract in reaction, a wave
begins to propagate itself down your
digestive tract. This phenomena is known
as peristalsis, and is responsible for moving
food through the many twists and turns of
the gut.
Smooth muscle, because of its ability to
contract and hold, is used for many function
in many places of the body. Besides those
listed above, smooth muscle is also
responsible for contracting the irises, raising
the small hairs on your arm, contracting the
many sphincters in your body, and even
moving fluids through organs by applying
pressure to them. While smooth muscle
doesn’t contract or release as quickly as
skeletal or cardiac muscle, it is much more
useful for providing consistent, elastic
tension.
(Yang cardiac muscle ada di lily halaman 10
yang histology of ventricular myocardia cell)
Disitu kea dijelasin bagian bagianny gt
Terus fungsinya dia buat memompa jantung,
tapi yang bedain dia dengan smooth muscle
itu:
The primary function of both muscle types is
to contract, and in both cases a contraction
begins with a characteristic flow
of ions across the cell membrane known as
an action potential. The action potential
subsequently triggers muscle contraction by
increasing the concentration
of calcium within the cytosol.
However, the mechanism by which calcium
concentrations within the cytosol rise differ
between skeletal and cardiac muscle. In
cardiac muscle, the action potential
comprises an inward flow of both sodium
and calcium ions. The flow of sodium ions is
rapid but very short-lived, while the flow of
calcium is sustained and gives the plateau
phase characteristic of cardiac muscle
action potentials. The comparatively small
flow of calcium through the L-type calcium
channels triggers a much larger release of
calcium from the sarcoplasmic reticulum in a
phenomenon known as calcium-induced
calcium release. In contrast, in skeletal
muscle, minimal calcium flows into the cell
during action potential and instead the
sarcoplasmic reticulum in these cells is
directly coupled to the surface membrane.
This difference can be illustrated by the
observation that cardiac muscle fibres
require calcium to be present in the solution
surrounding the cell in order to contract,
while skeletal muscle fibres will contract
without extracellular calcium.
During contraction of a cardiac muscle cell,
the long protein myofilaments oriented along
the length of the slide over each other in
what is known as the sliding filament
hypothesis. There are two kinds of
myofilaments, thick filaments composed of
the protein myosin, and thin filaments
composed of the
proteins actin, troponin and tropomyosin. As
the thick and thin filaments slide past each
other the cell becomes shorter and fatter. In
a mechanism known as crossbridge cycling,
calcium ions bind to the protein troponin,
which along with tropomyosin then uncover
key binding sites on actin. Myosin, in the
thick filament, can then bind to actin, pulling
the thick filaments along the thin filaments.
When the concentration of calcium within
the cell falls, troponin and tropomyosin once
again cover the binding sites on actin,
causing the cell to relax.
e. Describe the ultrastructure of
endothelium and junctions
- endothelial
the endothelial cell (EC) tightly monitors
the transport of plasma molecules,
employing bidirectional receptor-mediated
and receptor-independent transcytosis
and endocytosis, regulates the vascular
tone, synthesises and secretes a large
variety of factors, and is implicated in the
regulation of cell cholesterol, lipid
homeostasis, signal transduction, proteins interact both among themselves
immunity, inflammation and haemostasis. and with other molecules.
Ultrastructurally, besides the common set
of organelles, the characteristic features of
the ECs are the particularly high number
of vesicles (caveolae) endowed with
numerous receptors, transendothelial
channels, the specialised plasma membrane
microdomains of distinct chemistry, and
characteristic intercellular junctions. The
vascular endothelium, with its broad
spectrum of paracrine, endocrine and
autocrine functions, can be regarded as a
multifunctional organ and chief governor of
body homeostasis. The cells react
progressively to aggressive factors, at first
by modulation of the constitutive functions
(permeability, synthesis), followed by EC
dysfunction (loss, impairment or new
functions); if the insults persist (in time or
intensity), cell damage and death ultimately
occur. In conclusion, the ECs are daring
cells that have the functional-structural
attributes to adapt to the ever-changing
surrounding milieu, to use innate
mechanisms to confront and defend against
insults and to monitor and maintain the
body's homeostasis.

- junction
Intercellular junctions mediate adhesion and
communication between adjoining
endothelial and epithelial cells. In the
endothelium, junctional complexes comprise
tight junctions, adherens junctions, and gap
junctions. The expression and organization
of these complexes depend on the type of
vessels and the permeability requirements
of perfused organs. Gap junctions are
communication structures, which allow the
passage of small molecular weight solutes
between neighboring cells. Tight junctions
serve the major functional purpose of
providing a "barrier" and a "fence" within the
membrane, by regulating paracellular
permeability and maintaining cell polarity.
Adherens junctions play an important role in
contact inhibition of endothelial cell growth,
paracellular permeability to circulating
leukocytes and solutes. In addition, they are
required for a correct organization of new
vessels in angiogenesis. Extensive research
in the past decade has identified several
molecular components of the tight and
adherens junctions, including integral
membrane and intracellular proteins. These