Cellular Response Towards Steroid Hormones Biology Essay


The degree of cellular response toward a steroid hormone is proportional to the amount of hormone-receptor complexes formed. On the contrary, cellular response to a nonsteroid hormone functioning through a second messenger is amplified. Cellular response is amplified because the enzymes stimulated by a small number of hormone-receptor complexes are capable of catalyzing the formation of a large number of second messenger molecules. As a consequence of such amplification, cells are extremely responsive to alterations in nonsteroid hormone concentrations.

The ovaries synthesize and secrete the female sex hormones including estrogens and progesterone. The secretion of both estrogens and progesterone is regulated by Luteinizing Hormone and Follicle Stimulating Hormone, which are in turn regulated by Gonadotropin Releasing Hormone. Specifically, FSH stimulates estrogen production and secretion from the anterior pituitary, which is turn controlled by GnRH from the hypothalamus. Progesterone production is initiated by LH from the anterior pituitary, which is stimulated by GnRH from the hypothalamus.

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The hormonal secretions of the ovaries, hypothalamus, and the anterior pituitary play important roles in the female reproductive cycle. From puberty through menopause, interactions between these hormones result in a monthly cyclical pattern known as the menstrual cycle.

The reproductive cycle begins with FSH from the anterior pituitary, which promotes the development of the follicle. The follicle grows, and the granulose cells of the follicle begin producing and secreting estrogens. The estrogens are accountable for sustaining the secondary sex traits in addition to the thickening of the endometrium.

Midway through the cycle ovulation occurs. A mature ovarian follicle bursts and releases an ovum. Ovulation is caused by a surge in LH released from the anterior pituitary gland and is preceded by a peak in estrogen levels.

Following ovulation, LH induces the ruptured follicle to develop into the corpus luteum, which secretes estrogen and progesterone. Progesterone provokes changes in the uterus. Progesterone causes the glands of the endometrium to mature and produce secretions that prepare it for the implantation of an embryo. In this way, the endometrium grows to be more glandular and vascular. Progesterone and estrogen prevent secretion of FSH and LH from the anterior pituitary gland, and are essential for the maintenance of the endometrium.

If the ovum is not fertilized, the corpus luteum atrophies. The resulting drop in progesterone and estrogen levels causes the endometrium, with its superficial blood vessels, to slough off, giving rise to the menstrual flow. The anterior pituitary gland is no longer restrained and begins to secrete FSH and LH again as the reproductive cycle repeats. If fertilization does occur, the developing placenta produces human chorionic gonadotropin, maintaining the corpus luteum and the thus the supply of estrogen and progesterone that maintains the uterus until the placenta takes over production of these hormones.

The three phases of gastric secretion are the cephalic, gastric, and intestinal phases. Parasympathetic impulses of the nervous system and the gastrin hormone of the endocrine system are important in these phases as they enhance gastric secretion.

The cephalic phase starts prior to food reaching the stomach and perhaps prior to eating. At the sight, smell, taste, or thought of food, parasympathetic impulses functioning through the vagus nerves stimulate secretion of gastrin. The greater the appetite, the greater the stimulation.

The gastric phase begins as food goes into the stomach. Gastric secretion is stimulated from ingested food by the stomach stretching and by the pH of its contents rising. The presence of food and the swelling of the stomach wall activates a parasympathetic reflex. This causes the stomach to produce gastrin, stimulating additional gastric juice secretion. As food mixes with gastric juice, the pH of the contents rise, enhancing gastric secretion even further. It is important to note that acetylcholine, histamine, and gastrin are chemicals that stimulate gastric secretion in the gastric phase. These chemicals also stimulate the gastric glands to secrete pepsin and HCl. As ingested food is digested, food contents are emptied from the stomach, the pH drops, and the low pH stomach acid marks the ending of the gastric phase as the need for pepsin and HCl decreases.

The intestinal phase starts as digested food exits the stomach and goes into the small intestine. As additional chyme goes into the small intestine, gastric juice secretion is repressed by a sympathetic reflex that is activated by acid in the small intestine. Chyme also stimulates cells to release CCK, further suppressing gastric secretion and motility. Gastric secretion stops when chyme has enough HCl to bring its pH below 2. Food entering the small intestine and a low pH causes the release of local hormones secretin, cholecystokinin, and gastric inhibitory peptide to circulate to the gastric glands. These hormones inhibit gastric gland secretion, and block further digestive action.

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Hormones involved during the gastric and intestinal phases of digestion and absorption include gastrin, intestinal gastrin, cholecystokinin, and intestinal somatostatin.

Gastrin is a peptide hormone that stimulates the secretion of gastric juice by stomach cells. Gastrin also promotes the release of histamine, a chemical that further stimulates gastric secretion.

Intestinal gastrin is released as food contacts the intestinal wall and enhances the secretion of the gastric gland.

Fats and proteins in the intestine prompt the release of cholecystokinin. The release of CCK inhibits gastric motility, and causes the gall bladder to contract and release bile. It also causes the pancreas to release its fluid with a high digestive enzyme concentration.

Correspondingly, fats in the intestine activate the release of intestinal somatostatin, a hormone that further suppresses the release gastric juice. Together, intestinal somatostatin and CCK block further digestion.

(E) Insulin functions in lowering blood glucose levels by increasing the rate of glucose utilization. Insulin is released when blood glucose levels are high, allowing glucose to be taken up and used. On the contrary, glucagon raises blood glucose levels. Glucagon is released from the pancreas when blood glucose levels are low. In effect, glucagon instigates the liver to convert accumulated glycogen into glucose, letting it go into the bloodstream and raise blood glucose levels.

Thus, glucagon and insulin function as a feedback system, maintaining blood glucose levels at a steady level.

Growth hormone stimulates the body cells to grow and divide. GH also increases the movement of amino acids through cell membranes. Additionally, GH increases the rate by which cells use fats, and reduces the rate cells use carbohydrates. Therefore, dietary condition can effect GH control. For instance, additional GH is released during episodes of low blood glucose levels, and less GH is released during episodes of high blood glucose levels. GH is produced in the anterior pituitary, discharged into the blood stream, then promotes the liver to secrete IGF-1 in response to GH. Many of the effects of GH must be mediated by IGF-1. IGF-1 promotes body growth, especially muscle, cartilage, and bone.

(F) Glomerular filtration, tubular reabsorption, and tubular secretion occur to remove certain wastes from the body and to form urine.

Glomerular filtration is the beginning of urine formation. Glomerular filtration is the process where blood pressure pushes fluid all the way through the glomerular capillaries in the kidney and into the glomerular capsule. The glomerular capillaries filter small dissolved molecules, such as water and ions, out of the blood plasma and into the glomerular capsule. The glomerular capsule receives the resulting glomerular filtrate. As figure 20.16 in our book illustrates in great detail, the afferent arteriole delivers material into the glomerulus, supplying the blood plasma for the glomerular capillaries. As the blood plasma journeys through the capillaries it gets filtered through the very permeable capillary walls and makes its way into the renal tubule. It is this tubular fluid in the renal capsule that is excreted as urine. It is important to note that filtration can be affected by pressure. The filtration pressure is the force that moves material away from the glomerulus and into the glomerular capsule. In glomerular filtration, the major force that moves material via filtration inside the glomerular capillaries is hydrostatic blood pressure. Both osmotic pressure of blood plasma as well as the hydrostatic pressure in the glomerular capsule also affect filtration. Now, glomurular filtration rate may vary with the filtration pressure. Pressure changes as the diameters of the afferent and efferent arterioles change. For instance, as osmotic pressure in the glomerulus increases filtration rate decreases. Similarly, as hydrostatic pressure in the glomerular capsule increases, filtration decreases. Generally, glomerular filtration rate stays moderately constant due to autoregulation, a process that enables a tissue or organ to maintain constant blood flow when blood pressure is changing.

In tubular reabsorption, some materials from the glomerular filtrate are selectively reabsorbed back into the blood. The kidney selectively retrieves water, solutes, and other filtered solutes the body needs from tubular fluid and transfers them into the blood. Tubular reabsorption works with various forms of transport reabsorbing substances in certain parts of the renal tubule. Water is reabsorbed via osmosis, glucose and amino acids are reabsorbed via active transport, and proteins are reabsorbed via endocytosis. If the concentration of a certain substance in the glomerular filtrate surpasses its renal plasma threshold, the surplus is excreted as urine. The residual materials in the filtrate are concentrated while water is being reabsorbed.

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And in tubular secretion, some materials of blood plasma are selectively dispatched into tubules. Tubular secretion transfers material the body must elimiate quickly, such as hydrogen ions and specific toxins, out of the blood and into tubular fluid. Many of the substances, such as hydrogen ions and potassium ions, are actively secreted via active transport mechanisms.

Our bodies control tubular reabsorption and tubular secretion by regulating urine concentration and volume. The kidneys ability to maintain their internal environment relies on their potential to concentrate urine by means of reabsorbing significant amounts of water. The solute concentration of urine is managed, as most of the sodium ions are reabsorbed before urine is excreted. Sodium ions are concentrated in the renal medulla via a countercurrent mechanism. This countercurrent mechanism makes certain that the medullary interstitial fluid is hypertonic fluid, meaning that it looses water. When water removal is needed, no ADH is released, and fluid is excreted as urine as the distal convoluted tubule and collecting duct are impermeable to water. When water removal is not needed, ADH from the posterior pituitary gland is secreted, enhancing the permeability of the distal convoluted tubule and collecting duct, and enhancing water reabsorption.