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 cross-bridges (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.

Raymondos, K.; Panning, B.; Leuwer, M.; Brechelt, G.; Korte, T.; Niehaus, M.; Tebbenjohanns, J.; Piepenbrock, S. (2000). "Absorption and hemodynamic effects of airway administration of adrenaline in patients with severe cardiac disease". Ann. Intern. Med. 132 (10): 800803.

Sabyasachi Sircar (2007). Medical Physiology. Thieme Publishing Group. p.536.