Notes
37.3: Regulation of Body Processes
37.3.1: Hormonal Regulation of the Excretory System
The contrasting actions of antidiruetic hormone and aldosterone work to regulate the level of water in the body.
Learning Objective
Explain how the actions of different hormones regulate the excretory system
Key Points
- The hypothalamus monitors the amount of water in the body by sensing the concentration of electrolytes in the blood; a high concentration of electrolytes means that the level of water in the body is low.
- Antidiuretic hormone (ADH), produced by the hypothalamus and released by the posterior pituitary, causes more water to be retained by the kidneys when water levels in the body are low.
- ADH effects water retention by creating special channels for water, called aquaporins, inside the kidneys so that more water can be reabsorbed before it is excreted.
- Aldosterone, produced by the adrenal cortex, causes the retention of water in the body by increasing the levels of sodium and potassium ions in the blood, which causes the body to reabsorb more water.
- When blood pressure is low, the enzyme renin is released, which cleaves the protein angiotensinogen into angiotensin I, which is further converted into angiotensin II.
- Angiotensin II signals the adrenal cortex to release aldosterone, which then increases the retention of sodium ions, enhancing the secretion of postassium ions, resulting in water retention and an increase in blood pressure.
Key Terms
- aldosterone
a mineralocorticoid hormone, secreted by the adrenal cortex, that regulates the balance of sodium and potassium in the body
- aquaporin
any of a class of proteins that form pores in the membrane of biological cells
- electrolyte
any of the various ions (such as sodium or chloride) that regulate the electric charge on cells and the flow of water across their membranes
- mineralocorticoid
any of a group of steroid hormones, characterised by their similarity to aldosterone and their influence on salt and water metabolism
- renin
a circulating enzyme released by mammalian kidneys that converts angiotensinogen to angiotensin-I that plays a role in maintaining blood pressure
- osmoreceptor
a sensory receptor primarily found in the hypothalamus of most homeothermic organisms that detects changes in osmotic pressure
- antidiuretic hormone
a hormone secreted by the posterior pituitary gland that regulates the amount of water excreted by the kidneys
Hormonal Regulation of the Excretory System
Maintaining a proper water balance in the body is important to avoid dehydration or over-hydration (hyponatremia). The water concentration of the body is monitored by osmoreceptors in the hypothalamus, which detect the concentration of electrolytes in the extracellular fluid. The concentration of electrolytes in the blood rises when there is water loss caused by excessive perspiration, inadequate water intake, or low blood volume due to blood loss. An increase in blood electrolyte levels results in a neuronal signal being sent from the osmoreceptors in hypothalamic nuclei. The anterior pituitary is composed of glandular cells that secrete protein hormones. The pituitary gland has two components: anterior and posterior. The posterior pituitary is an extension of the hypothalamus. It is composed largely of neurons that are continuous with the hypothalamus.
Antidiuretic Hormone (ADH)
The hypothalamus produces a polypeptide hormone known as antidiuretic hormone (ADH), which is transported to and released from the posterior pituitary gland. The principal action of ADH is to regulate the amount of water excreted by the kidneys. As ADH (which is also known as vasopressin) causes direct water reabsorption from the kidney tubules, salts and wastes are concentrated in what will eventually be excreted as urine. The hypothalamus controls the mechanisms of ADH secretion, either by regulating blood volume or the concentration of water in the blood. Dehydration or physiological stress can cause an increase of osmolarity above threshold levels, which, in turn, raises ADH secretion and water retention, causing an increase in blood pressure. ADH travels in the bloodstream to the kidneys where it changes the kidneys to become more permeable to water by temporarily inserting water channels, aquaporins, into the kidney tubules. Water moves out of the kidney tubules through the aquaporins, reducing urine volume. The water is reabsorbed into the capillaries, lowering blood osmolarity back toward normal. As blood osmolarity decreases, a negative feedback mechanism reduces osmoreceptor activity in the hypothalamus; ADH secretion is reduced. ADH release can be reduced by certain substances, including alcohol, which can cause increased urine production and dehydration.
Chronic underproduction of ADH or a mutation in the ADH receptor results in diabetes insipidus. If the posterior pituitary does not release enough ADH, water cannot be retained by the kidneys and is lost as urine. This causes increased thirst, but water taken in is lost again and must be continually consumed. If the condition is not severe, dehydration may not occur, but severe cases can lead to electrolyte imbalances due to dehydration.
Another hormone responsible for maintaining electrolyte concentrations in extracellular fluids is aldosterone, a steroid hormone that is produced by the adrenal cortex. In contrast to ADH, which promotes the reabsorption of water to maintain proper water balance, aldosterone maintains proper water balance by enhancing Na+ reabsorption and K+ secretion from extracellular fluid of the cells in kidney tubules. Because it is produced in the cortex of the adrenal gland and affects the concentrations of minerals Na+ and K+, aldosterone is referred to as a mineralocorticoid, a corticosteroid that affects ion and water balance. Aldosterone release is stimulated by a decrease in blood sodium levels, blood volume, or blood pressure, or an increase in blood potassium levels. It also prevents the loss of Na+ from sweat, saliva, and gastric juice. The reabsorption of Na+ also results in the osmotic reabsorption of water, which alters blood volume and blood pressure.
Aldosterone production can be stimulated by low blood pressure, which triggers a sequence of chemical release . When blood pressure drops, the renin-angiotensin-aldosterone system (RAAS) is activated. Cells in the juxtaglomerular apparatus, which regulates the functions of the nephrons of the kidney, detect this and release renin. Renin, an enzyme, circulates in the blood, reacting with a plasma protein produced by the liver called angiotensinogen. When angiotensinogen is cleaved by renin, it produces angiotensin I, which is then converted into angiotensin II in the lungs. Angiotensin II functions as a hormone, causing the release of the hormone aldosterone by the adrenal cortex, resulting in increased Na+ reabsorption, water retention, and an increase in blood pressure. Angiotensin II, in addition to being a potent vasoconstrictor, also causes an increase in ADH and increased thirst, both of which help to raise blood pressure.
Action of aldosterone
ADH and aldosterone increase blood pressure and volume. Angiotensin II stimulates release of these hormones. Angiotensin II, in turn, is formed when renin cleaves angiotensin. This increases water retention and blood pressure.
37.3.2: Hormonal Regulation of the Reproductive System
Male and female gonads are regulated by FSH and LH from the pituitary; their production is stimulated by GnRH, secreted by the hypothalamus.
Learning Objective
Explain the regulation of the male and female reproductive systems
Key Points
- In males, FSH stimulates the production of sperm cells by signaling them to undergo meiosis, while in females, FSH stimulates the growth of the ovum inside the follicle of the ovary.
- In males, LH stimulates the Leydig cells within the testes to produce testosterone, which encourages sperm production and leads to secondary sexual characteristics.
- In females, LH plays a crucial role in signaling ovulation, as well as stimulating the production of other hormones that will prepare the body for pregnancy.
- Other hormones involved in the female reproductive system are oxytocin, which signals the uterus to contract during childbirth, and prolactin, which stimulates milk production.
Key Terms
- prolactin
a peptide gonadotrophic hormone secreted by the pituitary gland; it stimulates growth of the mammary glands and lactation in females
- inhibin
a peptide hormone, secreted by the gonads, which inhibits the secretion of follicle-stimulating hormone
- gonad
a sex organ that produces gametes; specifically, a testicle or ovary
- luteinizing hormone
a hormone, produced by part of the pituitary gland, that stimulates ovulation and the development of the corpus luteum in female mammals, and the production of androgens by male mammals
- follicle stimulating hormone
a gonadotropic glycoprotein hormone, secreted in the anterior pituitary, that stimulates the growth of ovarian follicles in female mammals, and induces spermatogenesis in male mammals
- gonadotropin-releasing hormone
a trophicpeptide responsible for the release of follicle stimulating hormone and lutenizing hormone from the anterior pituitary, synthesized and released from the hypothalamus
- androgen
the generic term for any natural or synthetic compound, usually a steroid hormone, that stimulates or controls the development and maintenance of masculine characteristics in vertebrates
Hormonal Regulation of the Reproductive System
Regulation of the reproductive system is a process that requires the action of hormones from the pituitary gland, the adrenal cortex, and the gonads. During puberty, in both males and females, the hypothalamus produces gonadotropin-releasing hormone (GnRH), which stimulates the production and release of follicle stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary gland. These hormones regulate the gonads (testes in males and ovaries in females); they are called gonadotropins. In both males and females, FSH stimulates gamete production and LH stimulates production of hormones by the gonads. An increase in gonad hormone levels inhibits GnRH production through a negative feedback loop .
The negative feedback loop of the male reproductive system
GnRH, secreted by the hypothalamus, stimulates the production of FSH and LH from the pituitary gland. These hormones encourage the development of sperm cells within the testicles, which then produce inhibin and inhibit the production of GnRH, FSH and LH in a negative feedback loop.
Regulation of the Male Reproductive System
At the pituitary, GnRH stimulates the synthesis and secretion of the gonadotropins, FSH and LH. These processes are controlled by the size and frequency of GnRH pulses, as well as by feedback from androgens and estrogens. Low-frequency GnRH pulses lead to FSH release, whereas high-frequency GnRH pulses stimulate LH release. In males, FSH stimulates primary spermatocytes to undergo the first division of meiosis, to form secondary spermatocytes, leading to the maturation of sperm cells. FSH also enhances the production of androgen-binding protein by the Sertoli cells of the testes by binding to FSH receptors on their basolateral membranes. FSH production is inhibited by the hormone inhibin, which is released by the testes.
LH stimulates production of the sex hormones (androgens) by the Leydig cells of the testes. It is also called interstitial-cell-stimulating hormone. The most widely-known androgen in males is testosterone, which promotes the production of sperm and masculine characteristics. The adrenal cortex also produces small amounts of testosterone precursor, although the role of this additional hormone production is not fully understood.
Regulation of the Female Reproductive System
In females, FSH stimulates development of egg cells (or ova) in structures called follicles. Follicle cells produce the hormone inhibin, which inhibits FSH production in the female reproductive system. LH also plays a role in the development of ova, induction of ovulation, and stimulation of estradiol and progesterone production by the ovaries . Estradiol and progesterone are steroid hormones that prepare the body for pregnancy. Estradiol produces secondary sex characteristics in females, while both estradiol and progesterone regulate the menstrual cycle.
Regulation of the female reproductive system
Hormonal regulation of the female reproductive system involves hormones from the hypothalamus, pituitary, and ovaries. GnRH secreted by the hypothalamus stimulates the release of FSH, which stimulates the growth of egg cells, and LH, which signals for the the ovulation of an egg from its follicle. The ovaries, in turn, secrete hormones that play a role in female sexual characteristics.
In addition to producing FSH and LH, the anterior portion of the pituitary gland also produces the hormone prolactin (PRL) in females. Prolactin stimulates the production of milk by the mammary glands, following childbirth. Prolactin levels are regulated by the hypothalamic hormones, prolactin-releasing hormone (PRH) and prolactin-inhibiting hormone (PIH) (which is now known to be dopamine). PRH stimulates the release of prolactin, while PIH inhibits it.
The posterior pituitary releases the hormone oxytocin, which stimulates uterine contractions during childbirth. The uterine smooth muscles are not very sensitive to oxytocin until late in pregnancy, when the number of oxytocin receptors in the uterus peaks. Stretching of tissues in the uterus and cervix stimulates oxytocin release during childbirth. Contractions increase in intensity as blood levels of oxytocin rise via a positive feedback mechanism until the birth is complete. Oxytocin also stimulates the contraction of myoepithelial cells around the milk-producing mammary glands. As these cells contract, milk is forced from the secretory alveoli into milk ducts and is ejected from the breasts in a milk ejection ("let-down") reflex. Oxytocin release is stimulated by the suckling of an infant, which triggers the synthesis of oxytocin in the hypothalamus and its release into circulation at the posterior pituitary.
37.3.3: Hormonal Regulation of Metabolism
The levels of glucose in the blood are regulated by the hormones insulin and glucagon from the pancreas, and T3 and T4 from the thyroid.
Learning Objective
Explain how the hormones glucagon and insulin regulate blood glucose
Key Points
- When blood glucose levels rise, insulin is secreted by the pancreas, lowering blood glucose by increasing its uptake in cells and stimulating the liver to convert glucose to glycogen, in which form it can be stored.
- If insulin secretion is impaired, it can result in diabetes mellitus: a disease in which blood glucose levels remain high, leading to excess glucose in the urine, increased urine output, and dehydration, among other symptoms.
- When blood glucose levels fall, glucagon is secreted by the pancreas, which increases blood glucose levels by stimulating the breakdown of glycogen into glucose and the creation of glucose from amino acids.
- The basal metabolic rate of the body is controlled by the hormones T3 and T4, produced by the thyroid gland in response to the thyroid stimulating hormone (TSH), produced by the anterior pituitary.
- T3 and T4 bind to receptors on the mitochondria, causing an increase in the production of ATP, as well as increase in the transcription of genes that help utilize glucose and produce ATP, resulting in higher metabolism of the cell.
Key Terms
- hyperthyroidism
the excessive production of hormones by the thyroid
- hypothyroidism
the disease state caused by insufficient production of thyroid hormone by the thyroid gland
- triiodothyronine
the most powerful thyroid hormone, affecting almost every process in the body, including body temperature, growth, and heart rate
- thyroxine
a hormone (an iodine derivative of tyrosine), produced by the thyroid gland, that regulates cell metabolism and growth
- gluconeogenesis
the metabolic process in which glucose is formed, mostly in the liver, from non-carbohydrate precursors
- glycogenolysis
the production of glucose-1-phosphate by splitting a glucose monomer from glycogen using inorganic phosphate
- hypoglycemia
a condition in which blood glucose levels are too low
- glycogen
a polysaccharide that is the main form of carbohydrate storage in animals; converted to glucose as needed
- glucagon
a hormone, produced by the pancreas, that opposes the action of insulin by stimulating the production of sugar
- insulin
a polypeptide hormone that regulates carbohydrate metabolism
Hormonal Regulation of Metabolism
Blood glucose levels vary widely over the course of a day as periods of food consumption alternate with periods of fasting. Insulin and glucagon are the two hormones primarily responsible for maintaining homeostasis of blood glucose levels. Additional regulation is mediated by the thyroid hormones.
Regulation of Blood Glucose Levels: Insulin and Glucagon
Cells of the body require nutrients in order to function. These nutrients are obtained through feeding. In order to manage nutrient intake, storing excess intake, and utilizing reserves when necessary, the body uses hormones to moderate energy stores. Insulin is produced by the beta cells of the pancreas, which are stimulated to release insulin as blood glucose levels rise (for example, after a meal is consumed). Insulin lowers blood glucose levels by enhancing the rate of glucose uptake and utilization by target cells, which use glucose for ATP production. It also stimulates the liver to convert glucose to glycogen, which is then stored by cells for later use. As insulin binds to its target cell via insulin receptors and signal transduction, it triggers the cell to incorporate glucose transport proteins into its membrane. This allows glucose to enter the cell, where it can be used as an energy source. These actions mediated by insulin cause blood glucose concentrations to fall, called a hypoglycemic, or "low sugar" effect, which inhibits further insulin release from beta cells through a negative feedback loop.
Impaired insulin function can lead to a condition called diabetes mellitus, which has many effects on the body . It can be caused by low levels of insulin production by the beta cells of the pancreas, or by reduced sensitivity of tissue cells to insulin. This prevents glucose from being absorbed by cells, causing high levels of blood glucose, or hyperglycemia (high sugar). High blood glucose levels make it difficult for the kidneys to recover all the glucose from nascent urine, resulting in glucose being lost in urine. High glucose levels also result in less water being reabsorbed by the kidneys, causing high amounts of urine to be produced; this may result in dehydration. Over time, high blood glucose levels can cause nerve damage to the eyes and peripheral body tissues, as well as damage to the kidneys and cardiovascular system. Oversecretion of insulin can cause hypoglycemia, low blood glucose levels. This causes insufficient glucose availability to cells, often leading to muscle weakness. It can sometimes cause unconsciousness or death if left untreated.
Diabetes mellitus
Diabetes mellitus can cause a wide range of symptoms, including nausea, vomiting, blurred vision, lethargy, a frequency in urination, and high levels of glucose in the urine.
When blood glucose levels decline below normal levels, for example between meals or when glucose is utilized during exercise, the hormone glucagon is released from the pancreas. Glucagon raises blood glucose levels, eliciting what is called a hyperglycemic effect, by stimulating the breakdown of glycogen to glucose in skeletal muscle cells and liver cells in a process called glycogenolysis. Glucose can then be utilized as energy by muscle cells and released into circulation by the liver cells. Glucagon also stimulates absorption of amino acids from the blood by the liver, which then converts them to glucose. This process of glucose synthesis is called gluconeogenesis. Rising blood glucose levels inhibit further glucagon release by the pancreas via a negative feedback mechanism. In this way, insulin and glucagon work together to maintain homeostatic glucose levels .
The regulation of blood glucose levels by insulin and glucagon
As the levels of glucose in the blood rise, insulin stimulates the cells to take up more glucose and signals the liver to convert the excess glucose to glycogen, a form in which it can be stored for later use. When the levels of glucose in the blood fall, glucagon responds by stimulating the breakdown of glycogen into glucose and signals the production of additional glucose from amino acids.
Regulation of Blood Glucose Levels: Thyroid Hormones
The basal metabolic rate, which is the amount of calories required by the body at rest, is determined by two hormones produced by the thyroid gland: thyroxine, also known as tetraiodothyronine or T4, and triiodothyronine, also known as T3. T3 and T4 release from the thyroid gland are stimulated by thyroid-stimulating hormone (TSH), which is produced by the anterior pituitary. These hormones affect nearly every cell in the body except for the adult brain, uterus, testes, blood cells, and spleen. They are transported across the plasma membrane of target cells where they bind to receptors on the mitochondria, resulting in increased ATP production. In the nucleus, T3and T4activate genes involved in energy production and glucose oxidation. This results in increased rates of metabolism and body heat production. This is known as the hormone's calorigenic effect.
Disorders can arise from both the underproduction and overproduction of thyroid hormones. Hypothyroidism, underproduction of the thyroid hormones, can cause a low metabolic rate leading to weight gain, sensitivity to cold, and reduced mental activity, among other symptoms. In children, hypothyroidism can cause cretinism, which can lead to mental retardation and growth defects. Hyperthyroidism, the overproduction of thyroid hormones, can lead to an increased metabolic rate, which may cause weight loss, excess heat production, sweating, and an increased heart rate.
37.3.4: Hormonal Control of Blood Calcium Levels
Blood levels of calcium are regulated by the parathyroid hormone, which acts on the bones, kidneys, and intestines to keep levels constant.
Learning Objective
Explain how blood calcium levels are regulated by parathyroid hormone
Key Points
- The parathyroid hormone (PTH), secreted by the parathyroid glands, is responsible for regulating blood calcium levels; it is released whenever blood calcium levels are low.
- PTH increases blood calcium levels by stimulating osteoclasts, which break down bone to release calcium into the blood stream.
- PTH increases blood calcium levels by increasing the amount of calcium resorbed by the kidneys before it can be excreted in the urine.
- PTH increases blood calcium levels by triggering the formation of calcitriol, which increases absorption of dietary calcium through the intestines.
- Calcitonin, a hormone produced by the thyroid, acts in opposition to PTH by inhibiting osteoclasts, stimulating osteoblasts, and increasing excretion of calcium into the urine by the kidneys.
Key Terms
- osteoclast
a large multinuclear cell associated with the resorption of bone
- calcitriol
the active metabolite 1,25-dihydroxycholecalciferol of vitamin D3 that is involved in the absorption of calcium
- hyperparathyroidism
an abnormal increase in parathyroid gland activity
- hypoparathyroidism
deficiency of parathyroid hormone
- calcitonin
a hormone, secreted by parenchymal cells, that regulates calcium and phosphate metabolism
- osteoblast
a mononucleate cell from which bone develops
- parathyroid hormone
a polypeptide hormone that is released by the chief cells of the parathyroid glands and is involved in raising the levels of calcium ions in the blood
Hormonal Control of Blood Calcium Levels
Regulation of blood calcium concentrations is important for generation of muscle contractions and nerve impulses, which are electrically stimulated. If calcium levels get too high, membrane permeability to sodium decreases and membranes become less responsive. If calcium levels get too low, membrane permeability to sodium increases and convulsions or muscle spasms may result.
Blood calcium levels are regulated by parathyroid hormone (PTH), which is produced by the parathyroid glands. PTH is released in response to low blood calcium levels. It increases calcium levels by targeting the skeleton, the kidneys, and the intestine . In the skeleton, PTH stimulates osteoclasts, which are cells that cause bone to be reabsorbed, releasing calcium from bone into the blood. PTH also inhibits osteoblasts, cells which deposit bone, reducing calcium deposition in bone. In the intestines, PTH increases dietary calcium absorption and in the kidneys, PTH stimulates re-absorption of the calcium. While PTH acts directly on the kidneys to increase calcium re-absorption, its effects on the intestine are indirect. PTH triggers the formation of calcitriol, an active form of vitamin D, which acts on the intestines to increase absorption of dietary calcium. PTH release is inhibited by rising blood calcium levels.
Regulation of blood calcium levels
Parathyroid hormone (PTH) is released in response to low blood calcium levels. It increases blood calcium levels by stimulating the resorption of bones, increasing calcium resorption in the kidneys, and indirectly increasing calcium absorption in the intestines.
Hyperparathyroidism results from an overproduction of PTH, which leads to excessive amounts of calcium being removed from bones and introduced into blood circulation. This may produce structural weakness of the bones, which can lead to deformation and fractures, plus nervous system impairment due to high blood calcium levels. Hypoparathyroidism, the underproduction of PTH, results in extremely low levels of blood calcium, which causes impaired muscle function and may result in tetany (severe sustained muscle contraction).
The hormone calcitonin, which is produced by the parafollicular (or C) cells of the thyroid, has the opposite effect on blood calcium levels as PTH. Calcitonin decreases blood calcium levels by inhibiting osteoclasts, stimulating osteoblasts, and stimulating calcium excretion by the kidneys. This results in calcium being added to the bones to promote structural integrity. Calcitonin is most important in children (when it stimulates bone growth), during pregnancy (when it reduces maternal bone loss), and during prolonged starvation (because it reduces bone mass loss). In healthy, nonpregnant, unstarved adults, the role of calcitonin is unclear.
37.3.5: Hormonal Regulation of Growth
Body growth is controlled by growth hormone (GH), produced by the anterior pituitary, and IGF-1, whose production is stimulated by GH.
Learning Objective
Describe the hormonal regulation of growth
Key Points
- Growth hormone binds to receptors on target cells, causing mature cartilage cells to divide, creating new cartilage tissue.
- Growth hormone stimulates the production of IGF-1, a hormone that increases the uptake of amino acids when they are at high levels in the blood, so that they can be formed into new proteins.
- Growth hormone-releasing hormone stimulates the production of GH by the anterior pituitary, while growth hormone-inhibiting hormone inhibits its production.
- When growth hormone production is abnormally low in children, it can result in pituitary dwarfism, in which individuals can be less than 30 inches tall; when growth hormone production is high in children, it can result in gigantism, in which individuals can be over 8 feet tall.
Key Terms
- gigantism
a condition caused by an over-production of growth hormone, resulting in excessive bone growth
- somatostatin
a polypeptide hormone, secreted by the pancreas, that inhibits the production of certain other hormones
- growth hormone
any polypeptide hormone secreted by the pituitary gland that promotes growth and regulates the metabolism of carbohydrates, proteins, and lipids
Hormonal Regulation of Growth
Hormonal regulation is required for the growth and replication of most cells in the body. Growth hormone (GH), produced by the anterior portion of the pituitary gland, accelerates the rate of protein synthesis, particularly in skeletal muscle and bones. Effects of growth hormone on the tissues of the body can generally be described as anabolic (building up). Like most other protein hormones, GH acts by interacting with a specific receptor on the surface of cells. Increased height during childhood is the most widely-known effect of GH. Height appears to be stimulated by at least two mechanisms: Because polypeptide hormones are not fat-soluble, they cannot penetrate cell membranes. Thus, GH exerts some of its effects by binding to receptors on target cells, where it activates a pathway that directly stimulates division and multiplication of chondrocytes of cartilage.
GH also stimulates, through another pathway, the production of insulin-like growth factor 1 (IGF-1), a hormone homologous to proinsulin. The liver, a major target organ of GH for this process, is the principal site of IGF-1 production. IGF-1 has growth-stimulating effects on a wide variety of tissues. IGFs stimulate the uptake of amino acids from the blood, allowing the formation of new proteins, particularly in skeletal muscle cells, cartilage cells, and other target cells . This is especially important after a meal, when glucose and amino acid concentration levels are high in the blood. GH levels are regulated by two hormones produced by the hypothalamus. GH release is stimulated by growth hormone-releasing hormone (GHRH) and is inhibited by growth hormone-inhibiting hormone (GHIH), also called somatostatin. IGF-1 also has stimulatory effects on osteoblast and chondrocyte activity to promote bone growth.
Effects of growth hormone
Growth hormone directly accelerates the rate of protein synthesis in skeletal muscle and bones. Insulin-like growth factor 1 (IGF-1) is activated by growth hormone and also allows formation of new proteins in muscle cells and bone.
A balanced production of growth hormone is critical for proper development. Underproduction of GH in adults does not appear to cause any abnormalities, but in children it can result in pituitary dwarfism, in which growth is reduced. Pituitary dwarfism is characterized by symmetric body formation. In some cases, individuals are under 30 inches in height. Oversecretion of growth hormone can lead to gigantism in children, causing excessive growth. In some documented cases, individuals can reach heights of over eight feet. In adults, excessive GH can lead to acromegaly, a condition in which there is enlargement of bones in the face, hands, and feet that are still capable of growth.
37.3.6: Hormonal Regulation of Stress
The adrenal glands respond to either short-term or long-term stressors by releasing different hormones that act differently on the body.
Learning Objective
Describe the role of the adrenal glands in the "fight-or-flight" response and the body's reaction to stress
Key Points
- When the body senses stress, the hypothalamus signals the adrenal medulla to release epinephrine or norepinephrine, or the anterior pituitary to release ACTH.
- In short-term stressful situations, such as when a threat is perceived, epinephrine (adrenaline) and norepinephrine (noradrenaline) are released to prepare the body for a "fight-or-flight" response.
- Epinephrine and norepinephrine act to provide a burst of energy to the body by stimulating the breakdown of glycogen into glucose, increasing the heart rate, and dilating the bronchioles.
- In long-term stress situations, such as when the body must deal with injury or illness, ACTH is released, stimulating the production of corticosteroids, which include glucocorticoids and mineralocorticoids.
- Glucocorticoids stimulate the synthesis of glucose and inhibit the immune system.
- Mineralocorticoids regulate ion and water balance of the body by stimulating the kidneys to excrete less water and sodium ions in the urine.
Key Terms
- mineralocorticoid
any of a group of steroid hormones, characterised by their similarity to aldosterone and their influence on salt and water metabolism
- corticosteroid
any of a group of steroid hormones, secreted by the adrenal cortex, that are involved in a large range of physiological systems
- norepinephrine
a neurotransmitter found in the locus coeruleus which is synthesized from dopamine
- epinephrine
(adrenaline) an amino acid-derived hormone secreted by the adrenal gland in response to stress
- catecholamine
any of a class of aromatic amines derived from pyrocatechol that are hormones produced by the adrenal gland
- glucocorticoid
any of a group of steroid hormones, produced by the adrenal cortex, that are involved in metabolism and have anti-inflammatory properties
- adrenocorticotropic hormone
a peptide hormone, secreted by the pituitary gland, that stimulates the secretion of other hormones
Hormonal Regulation of Stress
When a threat or danger is perceived, the body responds by releasing hormones that will ready it for the "fight-or-flight" response. The effects of this response are familiar to anyone who has been in a stressful situation: increased heart rate, dry mouth, and hair standing erect.
The sympathetic nervous system regulates the stress response via the hypothalamus. Stressful stimuli cause the hypothalamus to signal the adrenal medulla (which mediates short-term stress responses) via nerve impulses, and the adrenal cortex, which mediates long-term stress responses via the hormone adrenocorticotropic hormone (ACTH), which is produced by the anterior pituitary.
Short-term Stress Response
Interactions of the endocrine hormones have evolved to ensure the body's internal environment remains stable. Stressors are stimuli that disrupt homeostasis. The sympathetic division of the vertebrate autonomic nervous system has evolved the fight-or-flight response to counter stress-induced disruptions of homeostasis. In the initial alarm phase, the sympathetic nervous system stimulates an increase in energy levels through increased blood glucose levels. This prepares the body for physical activity that may be required to respond to stress: to either fight for survival or to flee from danger .
Fight-or-flight response
When an animal feels threatened, epinephrine and norepinephrine released by the adrenal medulla prepare the body to fight a threat or flee from it by breaking down stores of glycogen, which provides an immediate boost of energy.
When presented with a stressful situation, the body responds by calling for the release of hormones that provide a burst of energy. The hormones epinephrine (also known as adrenaline) and norepinephrine (also known as noradrenaline) are released by the adrenal medulla. Epinephrine and norepinephrine increase blood glucose levels by stimulating the liver and skeletal muscles to break down glycogen and by stimulating glucose release by liver cells. Additionally, these hormones increase oxygen availability to cells by increasing the heart rate and dilating the bronchioles. The hormones also prioritize body function by increasing blood supply to essential organs, such as the heart, brain, and skeletal muscles, while restricting blood flow to organs not in immediate need, such as the skin, digestive system, and kidneys. Epinephrine and norepinephrine are collectively called catecholamines.
Long-term Stress Response
Some stresses, such as illness or injury, can last for a long time. Glycogen reserves, which provide energy in the short-term response to stress, are exhausted after several hours and cannot meet long-term energy needs. If glycogen reserves were the only energy source available, neural functioning could not be maintained once the reserves became depleted due to the nervous system's high requirement for glucose. In this situation, the body has evolved a response to counter long-term stress through the actions of the glucocorticoids, which ensure that long-term energy requirements can be met. The glucocorticoids mobilize lipid and protein reserves, stimulate gluconeogenesis, conserve glucose for use by neural tissue, and stimulate the conservation of salts and water.
Long-term stress response differs from short-term stress response. The body cannot sustain the bursts of energy mediated by epinephrine and norepinephrine for long times. Instead, other hormones come into play. In a long-term stress response, the hypothalamus triggers the release of ACTH from the anterior pituitary gland. The adrenal cortex is stimulated by ACTH to release steroid hormones called corticosteroids. Corticosteroids turn on transcription of certain genes in the nuclei of target cells. They change enzyme concentrations in the cytoplasm and affect cellular metabolism.
There are two main corticosteroids: glucocorticoids, such as cortisol, and mineralocorticoids, such as aldosterone. These hormones target the breakdown of fat into fatty acids in the adipose tissue. The fatty acids are released into the bloodstream for other tissues to use for ATP production. The glucocorticoids primarily affect glucose metabolism by stimulating glucose synthesis. Glucocorticoids also have anti-inflammatory properties through inhibition of the immune system. For example, cortisone is used as an anti-inflammatory medication; however, it cannot be used long term as it increases susceptibility to disease due to its immune-suppressing effects. Mineralocorticoids function to regulate ion and water balance of the body. The hormone aldosterone stimulates the reabsorption of water and sodium ions in the kidney, which results in increased blood pressure and volume.
Hypersecretion of glucocorticoids can cause a condition known as Cushing's disease, characterized by a shifting of fat storage areas of the body. This can cause the accumulation of adipose tissue in the face and neck, and excessive glucose in the blood. Hyposecretion of the corticosteroids can cause Addison's disease, which may result in bronzing of the skin, hypoglycemia, and low electrolyte levels in the blood.
Attributions
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Hormonal Regulation of the Excretory System
- "OpenStax College, Biology. October 17, 2013." http://cnx.org/content/m44777/latest/?collection=col11448/latest. OpenStax CNX CC BY 3.0.
- "antidiuretic hormone." http://en.wiktionary.org/wiki/antidiuretic_hormone. Wiktionary CC BY-SA 3.0.
- "OpenStax College, Regulation of Body Processes. October 17, 2013." http://cnx.org/content/m44777/latest/Figure_37_03_01.jpg. OpenStax CNX CC BY 3.0.
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Hormonal Regulation of the Reproductive System
- "Follicle-stimulating hormone." http://en.wikipedia.org/wiki/Follicle-stimulating_hormone%23Effects_in_males. Wikipedia CC BY-SA 3.0.
- "gonadotropin-releasing hormone." http://en.wikipedia.org/wiki/gonadotropin-releasing%20hormone. Wikipedia CC BY-SA 3.0.
- "OpenStax College, Biology. October 17, 2013." http://cnx.org/content/m44777/latest/?collection=col11448/latest. OpenStax CNX CC BY 3.0.
- "follicle stimulating hormone." http://en.wiktionary.org/wiki/follicle_stimulating_hormone. Wiktionary CC BY-SA 3.0.
- "Hypothalamus pituitary testicles axis." http://en.wikipedia.org/wiki/File:Hypothalamus_pituitary_testicles_axis.png. Wikipedia CC BY-SA.
- "OpenStax College, Regulation of Body Processes. October 17, 2013." http://cnx.org/content/m44777/latest/Figure_37_03_03.jpg. OpenStax CNX CC BY 3.0.
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Hormonal Regulation of Metabolism
- "OpenStax College, Biology. October 17, 2013." http://cnx.org/content/m44777/latest/?collection=col11448/latest. OpenStax CNX CC BY 3.0.
- "OpenStax College, Regulation of Body Processes. October 17, 2013." http://cnx.org/content/m44777/latest/Figure_37_03_05.png. OpenStax CNX CC BY 3.0.
- "OpenStax College, Regulation of Body Processes. October 17, 2013." http://cnx.org/content/m44777/latest/Figure_37_03_04.jpg. OpenStax CNX CC BY 3.0.
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Hormonal Control of Blood Calcium Levels
- "OpenStax College, Biology. October 17, 2013." http://cnx.org/content/m44777/latest/?collection=col11448/latest. OpenStax CNX CC BY 3.0.
- "OpenStax College, Regulation of Body Processes. October 17, 2013." http://cnx.org/content/m44777/latest/Figure_37_03_06.jpg. OpenStax CNX CC BY 3.0.
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Hormonal Regulation of Growth
- "OpenStax College, Biology. October 17, 2013." http://cnx.org/content/m44777/latest/?collection=col11448/latest. OpenStax CNX CC BY 3.0.
- "OpenStax College, Regulation of Body Processes. October 17, 2013." http://cnx.org/content/m44777/latest/Figure_37_03_07.png. OpenStax CNX CC BY 3.0.
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Hormonal Regulation of Stress
- "OpenStax College, Biology. October 17, 2013." http://cnx.org/content/m44777/latest/?collection=col11448/latest. OpenStax CNX CC BY 3.0.
- "adrenocorticotropic hormone." http://en.wiktionary.org/wiki/adrenocorticotropic_hormone. Wiktionary CC BY-SA 3.0.
- "Gato enervado pola presencia dun can." http://en.wikipedia.org/wiki/File:Gato_enervado_pola_presencia_dun_can.jpg. Wikipedia CC BY.