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DISCUSSION

Smooth Muscle Structure


Smooth muscles are a large class of
muscles aside from striated muscles
(Campbell, 2005). They are termed
smooth due to the lack of sarcomeres and
they do not appear striated when viewed
under a microscope. Instead of sarcomeres,
the myofilaments of smooth muscles are
organized into bundles of filamnets attached
to dense bodies or connected at sites called
attachment plaques (Randall et al., 2002).
The functions of smooth muscles are more
independent of the nervous system
compared to striated muscles due to smooth
muscles being innervated by neurons of the
autonomic nervous system (Sircar, 2007).
Just like in striated muscles, actin and
myosin filaments are also present in smooth
muscles. A contraction happens when the
actin and myosin filaments slide past each
other while being pulled by myosin crossbridges (Raymondos et al., 2000).
Adrenaline
Epinephrine
(also
known
as
adrenaline) is part of a group of monoamines
called the catecholamines. It is produced at
the ends of sympathetic nerve fibres and in
the chromaffin cells of the adrenal medulla
from the amino acids tyrosine and
phenylalanine (Sircar, 2007).
In the experiment, initial detached
stomach contraction was at a 1 per minute
rate. Addition of adrenaline maintained the
contractions at 1 per minute. Further
addition of adrenaline decreased the
contraction to 0 per minute. This agrees with
the theoretical results, that adrenaline
Epinephrine is both a hormone and a
neurotransmitter, acting on nearly all body

tissues. The action of epinephrine


(contraction or relaxation) varies depending
on tissue type and tissue expression of
adrenergic receptors. High levels of
epinephrine in the lung and stomach induces
muscular relaxation. In contrast, high
epinephrine levels causes contraction of the
smooth muscle that lines most arterioles
through the facilitated entry of Ca2+, thereby
increasing heart rate (Raz et al., 1991).
The mode of action of epinephrine is
by binding to a variety of adrenergic
receptors. It is a nonselective agonist of all
adrenergic receptors, including the major
subtypes 1, 2, 1, 2, and 3. Epinephrine's
binding to different receptors triggers a
number of metabolic changes. For example,
binding to an -adrenergic receptor
stimulates glycogenolysis in the liver and
muscle, inhibits insulin secretion by the
pancreas, and stimulates glycolysis and
inhibits insulin-mediated glycogenesis in
muscle. In contrast, -adrenergic receptor
binding causes increased adrenocorticotropic
hormone (ACTH) secretion by the pituitary
gland, glucagon secretion in the pancreas,
and increased lipolysis by adipose tissue.
Altogether, these lead to increased blood
glucose and fatty acids, providing substrates
for energy production within cells
throughout the body (Raymondos et al.,
2000).
REFERENCES
Campbell, Neil A.; Reece, Jane B. (2005).
Biology. Benjamin Cummings. p. 1230.
Randall, D. J., Burggren, W. W., French, K.,
& Eckert, R. (2002). Eckert animal
physiology: Mechanisms and adaptations.
New York: W.H. Freeman and Co.
Raz, I; Katz, A; Spencer, MK (March 1991).
"Epinephrine inhibits insulin-mediated

glycogenesis but enhances glycolysis in


human skeletal muscle.". The American
journal of physiology 260 (3 Pt 1): E4305.

airway administration of adrenaline in


patients with severe cardiac disease". Ann.
Intern. Med. 132 (10): 800803.

Raymondos, K.; Panning, B.; Leuwer, M.;


Brechelt, G.; Korte, T.; Niehaus, M.;
Tebbenjohanns, J.; Piepenbrock, S. (2000).
"Absorption and hemodynamic effects of

Sabyasachi Sircar (2007). Medical


Physiology. Thieme Publishing Group.
p. 536.

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