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Regulation of Physiological Process by Thyroid Hormones - Essay Example

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The reporter states that hormones are chemical messengers that carry signals from one cell to another via the blood. Moreover, there are eight major endocrine glands in the body. They are pituitary gland, pineal gland, thyroid gland, thymus, adrenal glands, pancreas, ovary (in women) and testes (in men)…
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Regulation of Physiological Process by Thyroid Hormones
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Using TWO examples, explain how hormones regulate physiological processes. Hormones are chemical messengers that carry signals from one cell to another via the blood. They are produced by endocrine glands. There are eight major endocrine glands in the body. They are pituitary gland, pineal gland, thyroid gland, thymus, adrenal glands, pancreas, ovary (in women) and testes (in men). Hormones have a major role in the physiological processes in the body. Their functions include reproduction and sexual differentiation, development and growth, maintenance of the internal environment, and regulation of metabolism and nutrient supply (Nussey & Whitehead 2001). A single hormone may affect more than one of these functions. On the other hand, each function may be controlled by several hormones, which act in concert. The secretion of the hormones in a normal human being is mainly based on negative feedback control, most of which involves the hypothalamo-pituitary axis that detects changes in the concentration of hormones secreted by peripheral endocrine glands. The hormones may also be secreted in response to changes in a controlled variable (Nussey & Whitehead 2001). The following examples illustrate as to how hormones regulate physiological function. Regulation of physiological process by thyroid hormones The thyroid hormones, namely, thyroxine (T3) and tri-iodothyronine (T4) are secreted by the thyroid gland. They stimulate the oxygen consumption of most of the cells of the body, help in the regulation of lipid and carbohydrate metabolism, and are essential for normal growth and maturation. The thyroid hormones enter the cells after which T3 binds to the thyroid receptors in the nuclei. T4 binds, but not avidly. The thus formed hormone- receptor complex then binds to DNA via zinc fingers and affects the variety of different of different genes that code for enzymes which regulate cell function. The main physiological effect of thyroid hormones is calorigenic action (Ganong 2003). The hormones increase oxygen consumption of most of the tissues in the body except brain, testes, uterus, lymph nodes, spleen and anterior pituitary. The hormones also increase the metabolism of fatty acids. Due to increased calorigenic action, nitrogen excretion is increased and endogenous protein and fat stores are metabolized, which may lead to weight loss. The hormones also cause hepatic conversion of carotene to vitamin A. Other functions include increase in cardiac output by direct action on the heart and also by activating heat dissipation mechanisms. The pulse pressure and heart rate is also increased, thus shortening circulation time. In the central nervous system, the thyroid hormones increase responsiveness of the brain tissue to catecholamines, thus activating reticular activating system. The hormones also affect brain development and reflexes. They increase the rate of absorption of carbohydrate from the gastrointestinal tract. They are essential for bone growth and epiphyseal closure. These hormones are also essential for growth hormone production (Ganong 2003). The day-to-day maintenance of thyroid hormones secretion depends on the thyroid stimulating hormone (TSH) and thyrotropic releasing hormone (TRH). TSH is produced by the anterior pituitary and TRH by the hypothalamus. TRH is in turn influenced by various factors like cold (Ganong 2003). Regulation of physiological process by insulin Insulin is secreted by the organ pancreas. The physiological actions of insulin can be categorized as: rapid, intermediate and delayed. The rapid actions are those which occur within minutes and are mainly, increased transport of glucose, aminoacids and potassium ions into insulin sensitive cells. The intermediate actions are those which are seen within minutes after release of insulin. These are mainly stimulation of protein synthesis, inhibition of protein degradation, activation of glycolytic enzymes and glycogen synthase and inhibition of phosphorylase and gluconeogenic enzymes. The delayed actions are seen after hours of release. One of the main delayed action is increase in mRNAs for lipogenic and other enzymes (Ganong 2003). The main actions of insulin are seen on adipose tissue, skeletal, cardiac and smooth muscles and on the liver. In the adipose tissue, the insulin increases glucose entry, fatty acid synthesis, glycerol phosphate synthesis and triglyceride deposition. It activates lipoprotein lipase and inhibits hormone sensitive lipase. It also increases potassium uptake. In the muscle, glucose entry is increased. The hormone also increases glycogen synthesis, amino acid uptake, ketone uptake, potassium uptake and protein synthesis in the ribosomes. It decreases protein catabolism and release of gluconeogenic aminoacids. In the liver, insulin decreases ketogenesis and glucose output secondary to decreased gluconeogenesis and increased glycolysis. It also increases protein and lipid synthesis (Ganong 2003). Insulin acts by acting on the insulin receptors which are found on many different cells in the body. The insulin secretion is rather regulated by the glucose concentration in blood. It is secreted in primarily in response to elevated blood concentrations of glucose. The normal fasting blood glucose concentration in humans is 80 to 90 mg per 100 ml and is associated with very low levels of insulin secretion. Other stimuli which increase insulin secretion are some neural stimuli like sight and taste of food and increased blood concentrations of other fuel molecules, including amino acids and fatty acids (Ganong 2003). What do you understand by the term fluid electrolyte balance? Normally, in an adult, 60% of body weight is water which is present in various fluid compartments of the body namely, blood plasma, interstitial fluid and intracellular fluid. The blood plasma constitutes 5% of body weight and the interstitial fluid constitutes 15% of body weight. Both these together are called extracellular fluid. The intracellular fluid constitiutes 40% of body weight (Ganong 2003). These fluids have electrolytes in them. Electrolytes are minerals in the body that have an electric charge. These electrolytes are present in the blood, urine and body fluids. The main electrolytes are sodium, calcium, potassium, chlorine, phosphate and magnesium. It is essential to maintain a balance of fluids and electrolytes in the body for appropriate functioning of all the organs and maintenance of homeostasis of the body (Ganong 2003). The fluid electrolyte balance in the body is mainly maintained by the kidneys. The regulatory mechanisms in the kidney help adjust body fluid and electrolytes in situations as dehydration, blood loss, salt ingestion, and plain water ingestion. Water is maintained in the body by consumption in the form of foods, drinks and plain water; and by generation during catabolism. The water intake is regulated by various behavioral mechanisms like thirst and salt cravings. Water is lost from the body through the skin, lungs, feces and the kidneys. Kidneys play a major role in the regulation of water balance in the body. They conserve water by producing urine that is concentrated relative to plasma, or they get rid of the excess water by producing urine that is dilute relative to plasma (Ganong 2003). These functions are exercised by the hormone vasopressin (anti-diuretic hormone or ADH) which is secreted by the hypothalamus. This hormone is mainly secreted by the neurons of the suprachiasmatic nuclei. It is stored in the posterior pituitary. The hormone causes reabsorption of water by increasing the permeability of the collecting ducts of the kidney. This antidiuretic effect is mainly mediated by V-2 receptors. The ADH is discharged when the osmotic pressure of plasma increases beyond 285 mosm/kg. The secretion of this hormone is increased by special receptors in the hypothalamus that are sensitive to increasing plasma osmolarity and by stretch receptors in the aorta and carotid arteries, which are stimulated when blood pressure falls. The secretion is inhibited by stretch receptors in the atria of the heart, which are activated by a larger than normal volume of blood returning to the heart from the veins (Ganong 2003). Sodium is the most important electrolyte necessary for maintaining normal osmolality. It is the major solute in extracellular fluids, so it effectively determines the osmolarity of extracellular fluids. Regulation of osmolarity is achieved by balancing the intake and excretion of sodium with that of water. It is integrated with regulation of volume, because changes in water volume alone have diluting or concentrating effects on the bodily fluids. As discussed before, ADH plays a role in lowering osmolarity by increasing water reabsorption in the kidneys. Aldosterone, a steroid hormone produced by the adrenal cortex reabsorbs sodium from the distal nephron. Aldosterone increases the reabsorption of Na+ and water from urine and causes retention of Na+ and water in the extracellular fluid (ECF), thus expanding the ECF volume. This is primarily due to its action on the principal cells of the collecting ducts of the kidney. The Na+ is exchanged for K+ and H+. The renin-angiotensin system is a major regulator of aldosterone secretion. It plays an important role in regulating blood volume and systemic vascular resistance, which together influence cardiac output and arterial pressure (Klabunde, Cardiovascular Physiology Concepts). Renin is a proteolytic enzyme secreted by the juxta-glomerular cells (JG cells) in the kidney. . Its splits the decapepetide angiotensin-I from the amino terminal end of angiotensinogen which is found in the alpha-globulin fraction of the plasma. Angiotensin I is converted to angiotensin II by angiotensin converting enzyme. This enzyme is mainly located in the endothelial cells. Angiotensin I does not have much role. It is only a precursor of angiotensin II. Angiotensin II acts by AT-1 and AT-2 receptors. It stimulates zona glomerulosa cells by binding a plasma membrane receptor coupled to phospholipase C. This binding to the receptor leads to the activation of PKC and elevated intracellular Ca2+ levels. These events lead to increased P450ssc activity and increased production of aldosterone (“Steroids of the Adrenal Cortex”, MedEdPORTAL). The secretion of renin is regulated by several factors. The intrarenal baroreceptor system decreases renin secretion when the arteriolar pressure at the JG cells increases and it increases renin secretion when the pressure at the JG cells decreases. Renin secretion is also inversely proportional to the rate of transport and the amount of Na+ and Cl- across the macula densa of the renal tubule. It is also inversely proportional to plasma K+ level. Prostaglandins directly act on the JG cells and stimulate renin secretion. Increased angiotensin II and vasopressin also inhibit renin secretion whereas increased catecholamines increase renin secretion by acting on the beta-1 adrenergic receptors on the JG cells (Ganong, 2003). Renal artery hypotension (caused by systemic hypotension or renal artery stenosis also stimulates renin secretion (Klabunde, Cardiovascular Physiology Concepts). The fluid balance is thus maintained by various hormones in the body. References Ganong, W.F., 2003. Review of Medical Physiology. 21st edition. New York: Mc Graw Hill. Klabunde, R.E. Cardiovascular Physiology Concepts. Available from: from http://www.cvphysiology.com/Blood%20Pressure/BP015.htm [Accessed on 1 st Jan 2008] Insulin synthesis and Secretion. Available from: http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/pancreas/insulin.html [Accessed on 1 st Jan 2008] Nussey, S.S., Whitehead, S.A., 2001. Endocrinology- An Integrated Approach. Oxford: Taylor & Francis Steroids of the Adrenal Cortex. MedEdPORTAL. Available from: http://www.indstate.edu/thcme/mwking/steroid-hormones.html [Accessed on 1 st Jan 2008] Read More
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