D

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
Angiogenesis is a crucial process for embryonic and fetal development and organ growth. The
process is triggered by tissue hypoxia or insufficient oxygen tension leading to the new
development of blood vessels lined with endothelial cells. Angiogenesis is a tightly regulated
event that is balanced by pro- and antiangiogenic signals including integrins, chemokines,
angiopoietins, oxygen sensing agents, junctional molecules and endogenous inhibitors.[11]
The general outline of the process is

 activating signals binding to surface receptors of vascular endothelial cells.

 activated endothelial cells release proteases leading to the degradation of the basement
membrane
 endothelial cells are freed to migrate from the existing blood vessels and begin to proliferate
to form extensions towards the source of the angiogenic stimulus.

(ini w cari juga ya smooth muscle keanya si yg dimaksud cardiac muscle)

Smooth Muscle Definition

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.

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. Tests have shown
that these smooth muscles are stimulated by the presence or absence of oxygen, and modify the
veins to provide enough oxygen when it is low.

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 physiology of cardiac muscle shares many similarities with that of skeletal muscle. 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

(w gatau maksudnya ultrastructure apaan tapi keanya kayak selnya histo gtu)

- endothelial
Biology has revealed that form follows function or function creates the organ.
Translating this law at the cellular level, we may say that the ultrastructure follows
function or function creates the ultrastructure. The vascular endothelium is an
accurate illustration of this rule due to its numerous and many-sided functions carried
out by highly specialised cells, structurally equipped for their tasks. Occupying a
strategic position between the blood and tissues, 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, immunity,
inflammation and haemostasis. 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. In addition, by virtue of their number (-6 x
10(13)), aggregated mass (-1 kg), large surface area (-7,000 m2) and distribution
throughout the body, the ECs can perform all the assumed functions. 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 ECs exists in a high-risk position. 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 proteins interact both among themselves and with other molecules. Here, we
review the individual molecules of junctions and their complex network of interactions. We
also emphasize how the molecular architectures and interactions may represent a
mechanistic basis for the function and regulation of junctions, focusing on junction assembly
and permeability regulation. Finally, we analyze in vivo studies and highlight information that
specifically relates to the role of junctions in vascular endothelial cells.

(Gaketemu gambarnya aga gapaham si)