Power Point Lecture Slides prepared by Barbara Heard
Power. Point® Lecture Slides prepared by Barbara Heard, Atlantic Cape Community Ninth Edition College Human Anatomy & Physiology CHAPTER 16 The Endocrine System: Part A © Annie Leibovitz/Contact Press Images © 2013 Pearson Education, Inc.
Endocrine System: Overview • Acts with nervous system to coordinate and integrate activity of body cells • Influences metabolic activities via hormones transported in blood • Response slower but longer lasting than nervous system • Endocrinology – Study of hormones and endocrine organs © 2013 Pearson Education, Inc.
Endocrine System: Overview • Controls and integrates – Reproduction – Growth and development – Maintenance of electrolyte, water, and nutrient balance of blood – Regulation of cellular metabolism and energy balance – Mobilization of body defenses © 2013 Pearson Education, Inc.
Endocrine System: Overview • Exocrine glands – Nonhormonal substances (sweat, saliva) – Have ducts to carry secretion to membrane surface • Endocrine glands – Produce hormones – Lack ducts © 2013 Pearson Education, Inc.
Endocrine System: Overview • Endocrine glands: pituitary, thyroid, parathyroid, adrenal, and pineal glands • Hypothalamus is neuroendocrine organ • Some have exocrine and endocrine functions – Pancreas, gonads, placenta • Other tissues and organs that produce hormones – Adipose cells, thymus, and cells in walls of small intestine, stomach, kidneys, and heart © 2013 Pearson Education, Inc.
Figure 16. 1 Location of selected endocrine organs of the body. Pineal gland Hypothalamus Pituitary gland Thyroid gland Parathyroid glands (on dorsal aspect of thyroid gland) Thymus Adrenal glands Pancreas Gonads • Ovary (female) • Testis (male) © 2013 Pearson Education, Inc.
Chemical Messengers • Hormones: long-distance chemical signals; travel in blood or lymph • Autocrines: chemicals that exert effects on same cells that secrete them • Paracrines: locally acting chemicals that affect cells other than those that secrete them • Autocrines and paracrines are local chemical messengers; not considered part of endocrine system © 2013 Pearson Education, Inc.
Chemistry of Hormones • Two main classes – Amino acid-based hormones • Amino acid derivatives, peptides, and proteins – Steroids • Synthesized from cholesterol • Gonadal and adrenocortical hormones © 2013 Pearson Education, Inc.
Mechanisms of Hormone Action • Hormones act at receptors in one of two ways, depending on their chemical nature and receptor location 1. Water-soluble hormones (all amino acid– based hormones except thyroid hormone) • • • © 2013 Pearson Education, Inc. Act on plasma membrane receptors Act via G protein second messengers Cannot enter cell
Mechanisms of Hormone Action 2. Lipid-soluble hormones (steroid and thyroid hormones) • • © 2013 Pearson Education, Inc. Act on intracellular receptors that directly activate genes Can enter cell
Figure 16. 2 Cyclic AMP second-messenger mechanism of water-soluble hormones. Slide 1 Recall from Chapter 3 that G protein signaling mechanisms are like a molecular relay race. Hormone Receptor G protein Enzyme 2 nd (1 st messenger) messenger 1 Hormone (1 st messenger) binds receptor. Extracellular fluid Adenylate cyclase G protein (Gs) Receptor 5 c. AMP activates protein kinases. c. AMP GTP ATP GDP Inactive protein kinase GTP Active protein kinase Triggers responses of target cell (activates enzymes, stimulates cellular secretion, opens ion channel, etc. ) Cytoplasm 2 Receptor activates G protein (Gs). © 2013 Pearson Education, Inc. 3 G protein activates adenylate cyclase. 4 Adenylate cyclase converts ATP to c. AMP (2 nd messenger).
Figure 16. 3 Direct gene activation mechanism of lipid-soluble hormones. Extracellular fluid Steroid hormone Plasma membrane Cytoplasm Receptor protein Nucleus Slide 1 1 The steroid hormone diffuses through the plasma membrane and binds an intracellular receptor. Receptorhormone complex 2 The receptorhormone complex enters the nucleus. Receptor Binding region DNA m. RNA 3 The receptor- hormone complex binds a specific DNA region. 4 Binding initiates transcription of the gene to m. RNA. 5 The m. RNA directs protein synthesis. New protein © 2013 Pearson Education, Inc.
Target Cell Specificity • Target cells must have specific receptors to which hormone binds, for example – ACTH receptors found only on certain cells of adrenal cortex – Thyroxin receptors are found on nearly all cells of body © 2013 Pearson Education, Inc.
Target Cell Activation • Hormones influence number of their receptors – Up-regulation—target cells form more receptors in response to low hormone levels – Down-regulation—target cells lose receptors in response to high hormone levels © 2013 Pearson Education, Inc.
Figure 16. 4 a Three types of endocrine gland stimuli. Slide 1 Humoral Stimulus Hormone release caused by altered levels of certain critical ions or nutrients. Capillary (low Ca 2+ in blood) Thyroid gland (posterior view) Parathyroid glands PTH Stimulus: Low concentration of Ca 2+ in capillary blood. Response: Parathyroid glands secrete parathyroid hormone (PTH), which increases blood Ca 2+. © 2013 Pearson Education, Inc.
Neural Stimuli • Nerve fibers stimulate hormone release – Sympathetic nervous system fibers stimulate adrenal medulla to secrete catecholamines © 2013 Pearson Education, Inc.
Figure 16. 4 b Three types of endocrine gland stimuli. Slide 1 Neural Stimulus Hormone release caused by neural input. CNS (spinal cord) Preganglionic sympathetic fibers Medulla of adrenal gland Capillary Stimulus: Action potentials in preganglionic sympathetic fibers to adrenal medulla. Response: Adrenal medulla cells secrete epinephrine and norepinephrine. © 2013 Pearson Education, Inc.
Hormonal Stimuli • Hormones stimulate other endocrine organs to release their hormones – Hypothalamic hormones stimulate release of most anterior pituitary hormones – Anterior pituitary hormones stimulate targets to secrete still more hormones – Hypothalamic-pituitary-target endocrine organ feedback loop: hormones from final target organs inhibit release of anterior pituitary hormones © 2013 Pearson Education, Inc.
Figure 16. 4 c Three types of endocrine gland stimuli. Hormonal Stimulus Hormone release caused by another hormone (a tropic hormone). Hypothalamus Anterior pituitary gland Thyroid gland Adrenal Gonad cortex (Testis) Stimulus: Hormones from hypothalamus. Response: Anterior pituitary gland secretes hormones that stimulate other endocrine glands to secrete hormones. © 2013 Pearson Education, Inc. Slide 1
Nervous System Modulation • Nervous system modifies stimulation of endocrine glands and their negative feedback mechanisms – Example: under severe stress, hypothalamus and sympathetic nervous system activated • body glucose levels rise • Nervous system can override normal endocrine controls © 2013 Pearson Education, Inc.
Duration of Hormone Activity • Limited – Ranges from 10 seconds to several hours – Effects may disappear as blood levels drop – Some persist at low blood levels © 2013 Pearson Education, Inc.
Interaction of Hormones at Target Cells • Multiple hormones may act on same target at same time – Permissiveness: one hormone cannot exert its effects without another hormone being present – Synergism: more than one hormone produces same effects on target cell amplification – Antagonism: one or more hormones oppose(s) action of another hormone © 2013 Pearson Education, Inc.
The Pituitary Gland Hypothalamus • Pituitary gland (hypophysis) has two major lobes – Posterior pituitary (lobe) • Neural tissue – Anterior pituitary (lobe) (adenohypophysis) • Glandular tissue © 2013 Pearson Education, Inc.
Figure 16. 5 a The hypothalamus controls release of hormones from the pituitary gland in two different ways (1 of 2). Slide 1 Paraventricular nucleus Hypothalamus Posterior lobe of pituitary Optic chiasma Infundibulum (connecting stalk) Hypothalamichypophyseal tract Supraoptic nucleus Inferior hypophyseal artery Axon terminals 2 Oxytocin and ADH are transported down the axons of the hypothalamic- hypophyseal tract to the posterior pituitary. 3 Oxytocin and ADH are stored in axon terminals in the posterior pituitary. Posterior lobe of pituitary Oxytocin ADH © 2013 Pearson Education, Inc. 1 Hypothalamic neurons synthesize oxytocin or antidiuretic hormone (ADH). 4 When hypothalamic neurons fire, action potentials arriving at the axon terminals cause oxytocin or ADH to be released into the blood.
Figure 16. 5 b The hypothalamus controls release of hormones from the pituitary gland in two different ways (2 of 2). Slide 1 Hypothalamus Anterior lobe of pituitary Superior hypophyseal artery 2 Hypothalamic hormones travel through portal veins to the anterior pituitary where they stimulate or inhibit release of hormones made in the anterior pituitary. 3 In response to releasing hormones, the anterior pituitary secretes hormones into the secondary capillary plexus. This in turn empties into the general circulation. GH, TSH, ACTH, FSH, LH, PRL Anterior lobe of pituitary © 2013 Pearson Education, Inc. Hypothalamic neurons synthesize GHRH, GHIH, TRH, CRH, Gn. RH, PIH. 1 When appropriately stimulated, hypothalamic neurons secrete releasing or inhibiting hormones into the primary capillary plexus. Hypophyseal portal system • Primary capillary plexus • Hypophyseal portal veins • Secondary capillary plexus A portal system is two capillary plexuses (beds) connected by veins.
Posterior Pituitary and Hypothalamic Hormones • Oxytocin and ADH – Each composed of nine amino acids – Almost identical – differ in two amino acids © 2013 Pearson Education, Inc.
ADH • Diabetes insipidus – ADH deficiency due to hypothalamus or posterior pituitary damage – Must keep well-hydrated • Syndrome of inappropriate ADH secretion (SIADH) – Retention of fluid, headache, disorientation – Fluid restriction; blood sodium level monitoring © 2013 Pearson Education, Inc.
Anterior Pituitary Hormones • Growth hormone (GH) • Thyroid-stimulating hormone (TSH) or thyrotropin • Adrenocorticotropic hormone (ACTH) • Follicle-stimulating hormone (FSH) • Luteinizing hormone (LH) • Prolactin (PRL) © 2013 Pearson Education, Inc.
Growth Hormone (GH, or Somatotropin) • Produced by somatotropic cells • Direct actions on metabolism – Increases blood levels of fatty acids; encourages use of fatty acids for fuel; protein synthesis – Decreases rate of glucose uptake and metabolism – conserving glucose – Glycogen breakdown and glucose release to blood (anti-insulin effect) © 2013 Pearson Education, Inc.
Homeostatic Imbalances of Growth Hormone • Hypersecretion – In children results in gigantism – In adults results in acromegaly • Hyposecretion – In children results in pituitary dwarfism © 2013 Pearson Education, Inc.
Figure 16. 6 Growth-promoting and metabolic actions of growth hormone (GH). Inhibits GHRH release Stimulates GHIH release Feedback Anterior pituitary Hypothalamus secretes growth hormone–releasing hormone (GHRH), and GHIH (somatostatin) Inhibits GH synthesis and release Growth hormone (GH) Direct actions Indirect actions (metabolic, anti-insulin) (growthpromoting) Liver and other tissues Produce Insulin-like growth factors (IGFs) Effects Skeletal Extraskeletal Fat metabolism Carbohydrate metabolism Increases, stimulates Reduces, inhibits Increased cartilage formation and skeletal growth © 2013 Pearson Education, Increased protein synthesis, and cell growth and proliferation Increased fat breakdown and release Increased blood glucose and other anti-insulin effects Initial stimulus Physiological response Result
Figure 16. 7 Disorders of pituitary growth hormone. © 2013 Pearson Education, Inc.
Thyroid-stimulating Hormone (Thyrotropin) • Produced by thyrotropic cells of anterior pituitary • Stimulates normal development and secretory activity of thyroid • Release triggered by thyrotropin-releasing hormone from hypothalamus • Inhibited by rising blood levels of thyroid hormones that act on pituitary and hypothalamus © 2013 Pearson Education, Inc.
Figure 16. 8 Regulation of thyroid hormone secretion. Hypothalamus TRH Anterior pituitary TSH Thyroid gland Thyroid hormones Target cells © 2013 Pearson Education, Inc. Stimulates Inhibits
Adrenocorticotropic Hormone (Corticotropin) • Regulation of ACTH release – Triggered by hypothalamic corticotropinreleasing hormone (CRH) in daily rhythm – Internal and external factors such as fever, hypoglycemia, and stressors can alter release of CRH © 2013 Pearson Education, Inc.
Gonadotropins • Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) • Secreted by gonadotropic cells of anterior pituitary • FSH stimulates gamete (egg or sperm) production • LH promotes production of gonadal hormones • Absent from the blood in prepubertal boys and girls © 2013 Pearson Education, Inc.
Thyroid Gland • Two lateral lobes connected by median mass called isthmus • Composed of follicles that produce glycoprotein thyroglobulin • Colloid (fluid with thyroglobulin + iodine) fills lumen of follicles and is precursor of thyroid hormone • Parafollicular cells produce the hormone calcitonin © 2013 Pearson Education, Inc.
Thyroid Hormone (TH) • Actually two related compounds – T 4 (thyroxine); has 2 tyrosine molecules + 4 bound iodine atoms – T 3 (triiodothyronine); has 2 tyrosines + 3 bound iodine atoms • Affects virtually every cell in body © 2013 Pearson Education, Inc.
Thyroid Hormone • Major metabolic hormone • Increases metabolic rate and heat production (calorigenic effect) • Regulation of tissue growth and development – Development of skeletal and nervous systems – Reproductive capabilities • Maintenance of blood pressure © 2013 Pearson Education, Inc.
Figure 16. 10 Synthesis of thyroid hormone. Slide 1 Thyroid follicular cells Colloid 1 Thyroglobulin is synthesized and discharged into the follicle lumen. Tyrosines (part of thyroglobulin molecule) Capillary 4 Iodine is attached to tyrosine in colloid, forming DIT and MIT. Golgi apparatus Rough ER Iodine 3 Iodide is oxidized to iodine. 2 Iodide (I–) is trapped (actively transported in). Iodide (I−) T 4 T 3 Lysosome DIT MIT Thyroglobulin colloid 5 Iodinated tyrosines are linked together to form T 3 and T 4 T 3 To peripheral tissues © 2013 Pearson Education, Inc. 6 Thyroglobulin colloid is endocytosed and combined with a lysosome. 7 Lysosomal enzymes cleave T 4 and T 3 from thyroglobulin and hormones diffuse into bloodstream. Colloid in lumen of follicle
Transport and Regulation of TH • T 4 and T 3 transported by thyroxine-binding globulins (TBGs) • Both bind to target receptors, but T 3 is ten times more active than T 4 • Peripheral tissues convert T 4 to T 3 © 2013 Pearson Education, Inc.
Figure 16. 8 Regulation of thyroid hormone secretion. Hypothalamus TRH Anterior pituitary TSH Thyroid gland Thyroid hormones Target cells © 2013 Pearson Education, Inc. Stimulates Inhibits
Homeostatic Imbalances of TH • Hyposecretion in adults—myxedema; goiter if due to lack of iodine • Hyposecretion in infants—cretinism • Hypersecretion—most common type is Graves' disease © 2013 Pearson Education, Inc.
Figure 16. 11 Thyroid disorders. © 2013 Pearson Education, Inc.
Calcitonin • • Produced by parafollicular (C) cells No known physiological role in humans Antagonist to parathyroid hormone (PTH) At higher than normal doses – Inhibits osteoclast activity and release of Ca 2+ from bone matrix – Stimulates Ca 2+ uptake and incorporation into bone matrix © 2013 Pearson Education, Inc.
Parathyroid Glands • Four to eight tiny glands embedded in posterior aspect of thyroid • Contain oxyphil cells (function unknown) and parathyroid cells that secrete parathyroid hormone (PTH) or parathormone • PTH—most important hormone in Ca 2+ homeostasis © 2013 Pearson Education, Inc.
Figure 16. 12 The parathyroid glands. Pharynx (posterior aspect) Capillary Thyroid gland Parathyroid glands Esophagus Trachea © 2013 Pearson Education, Inc. Parathyroid cells (secrete parathyroid hormone) Oxyphil cells
Figure 16. 13 Effects of parathyroid hormone on bone, the kidneys, and the intestine. Hypocalcemia (low blood Ca 2+) PTH release from parathyroid gland Osteoclast activity in bone causes Ca 2+ and PO 43 - release into blood Ca 2+ reabsorption in kidney tubule Activation of vitamin D by kidney Ca 2+ absorption from food in small intestine Ca 2+ in blood Initial stimulus Physiological response © 2013 Pearson Education, Inc. Result
Homeostatic Imbalances of PTH • Hyperparathyroidism due to tumor – Bones soften and deform – Elevated Ca 2+ depresses nervous system and contributes to formation of kidney stones • Hypoparathyroidism following gland trauma or removal or dietary magnesium deficiency – Results in tetany, respiratory paralysis, and death © 2013 Pearson Education, Inc.
Adrenal (Suprarenal) Glands • Paired, pyramid-shaped organs atop kidneys • Structurally and functionally are two glands in one – Adrenal medulla—nervous tissue; part of sympathetic nervous system – Adrenal cortex—three layers of glandular tissue that synthesize and secrete corticosteroids © 2013 Pearson Education, Inc.
Figure 16. 14 Microscopic structure of the adrenal gland. Hormones secreted Zona glomerulosa Aldosterone Zona fasciculata Cortex Adrenal gland • Medulla • Cortex Capsule Cortisol androgens Kidney Medulla Zona reticularis Adrenal medulla Drawing of the histology of the adrenal cortex and a portion of the adrenal medulla © 2013 Pearson Education, Inc. Epinephrine and norepinephrine Photomicrograph (115 x)
Homeostatic Imbalances of Aldosterone • Aldosteronism—hypersecretion due to adrenal tumors – Hypertension and edema due to excessive Na+ – Excretion of K+ leading to abnormal function of neurons and muscle © 2013 Pearson Education, Inc.
Glucocorticoids • Keep blood glucose levels relatively constant • Maintain blood pressure by increasing action of vasoconstrictors • Cortisol (hydrocortisone) – Only one in significant amounts in humans • Cortisone • Corticosterone © 2013 Pearson Education, Inc.
Homeostatic Imbalances of Glucocorticoids • Hypersecretion—Cushing's syndrome/disease – Depresses cartilage and bone formation – Inhibits inflammation – Depresses immune system – Disrupts cardiovascular, neural, and gastrointestinal function • Hyposecretion—Addison's disease – Also involves deficits in mineralocorticoids • Decrease in glucose and Na+ levels • Weight loss, severe dehydration, and hypotension © 2013 Pearson Education, Inc.
Figure 16. 16 The effects of excess glucocorticoid. Patient before onset. © 2013 Pearson Education, Inc. Same patient with Cushing's syndrome. The white arrow shows the characteristic "buffalo hump" of fat on the upper back.
Gonadocorticoids (Sex Hormones) • Most weak androgens (male sex hormones) converted to testosterone in tissue cells, some to estrogens • May contribute to – Onset of puberty – Appearance of secondary sex characteristics – Sex drive in women – Estrogens in postmenopausal women © 2013 Pearson Education, Inc.
Gonadocorticoids • Hypersecretion – Adrenogenital syndrome (masculinization) – Not noticeable in adult males – Females and prepubertal males • Boys – reproductive organs mature; secondary sex characteristics emerge early • Females – beard, masculine pattern of body hair; clitoris resembles small penis © 2013 Pearson Education, Inc.
Adrenal Medulla • Medullary chromaffin cells synthesize epinephrine (80%) and norepinephrine (20%) • Effects – Vasoconstriction – Increased heart rate – Increased blood glucose levels – Blood diverted to brain, heart, and skeletal muscle © 2013 Pearson Education, Inc.
Adrenal Medulla • Hypersecretion – Hyperglycemia, increased metabolic rate, rapid heartbeat and palpitations, hypertension, intense nervousness, sweating • Hyposecretion – Not problematic – Adrenal catecholamines not essential to life © 2013 Pearson Education, Inc.
Figure 16. 17 Stress and the adrenal gland. Short-term stress Prolonged stress Stress Nerve impulses Hypothalamus CRH (corticotropinreleasing hormone) Spinal cord Corticotropic cells of anterior pituitary To target in blood Preganglionic sympathetic fibers Adrenal medulla (secretes amino acid– based hormones) Catecholamines (epinephrine and norepinephrine) Short-term stress response • Heart rate increases • Blood pressure increases • Bronchioles dilate • Liver converts glycogen to glucose and releases glucose to blood • Blood flow changes, reducing digestive system activity and urine output • Metabolic rate increases © 2013 Pearson Education, Inc. ACTH Mineralocorticoids Adrenal cortex (secretes steroid hormones) Glucocorticoids Long-term stress response • Kidneys retain • Proteins and fats converted sodium and water to glucose or broken down for energy • Blood volume and • Blood glucose increases blood pressure • Immune system rise supressed
Pineal Gland • Small gland hanging from roof of third ventricle • Pinealocytes secrete melatonin, derived from serotonin • Melatonin may affect – Timing of sexual maturation and puberty – Day/night cycles – Physiological processes that show rhythmic variations (body temperature, sleep, appetite) – Production of antioxidant and detoxification molecules in cells © 2013 Pearson Education, Inc.
Pancreas • Triangular gland partially behind stomach • Has both exocrine and endocrine cells – Acinar cells (exocrine) produce enzyme-rich juice for digestion – Pancreatic islets (islets of Langerhans) contain endocrine cells • Alpha ( ) cells produce glucagon (hyperglycemic hormone) • Beta ( ) cells produce insulin (hypoglycemic hormone) © 2013 Pearson Education, Inc.
Figure 16. 18 Photomicrograph of differentially stained pancreatic tissue. Pancreatic islet • (Glucagonproducing) cells • (Insulinproducing) cells Pancreatic acinar cells (exocrine) © 2013 Pearson Education, Inc.
Glucagon • Major target—liver • Causes increased blood glucose levels • Effects – Glycogenolysis—breakdown of glycogen to glucose – Gluconeogenesis—synthesis of glucose from lactic acid and noncarbohydrates – Release of glucose to blood © 2013 Pearson Education, Inc.
Insulin • Effects of insulin – Lowers blood glucose levels – Enhances membrane transport of glucose into fat and muscle cells – Inhibits glycogenolysis and gluconeogenesis – Participates in neuronal development and learning and memory • Not needed for glucose uptake in liver, kidney or brain © 2013 Pearson Education, Inc.
Figure 16. 19 Insulin and glucagon from the pancreas regulate blood glucose levels. Stimulates glucose uptake by cells Tissue cells Insulin Stimulates glycogen formationw Pancreas Glucose Glycogen Blood glucose falls to normal range. Liver IMB AL Stimulus Blood glucose level AN CE BALANCE: Normal blood glucose level (about 90 mg/100 ml) Stimulus IMB AL Blood glucose rises to normal range. AN CE Blood glucose level Pancreas Glucose Glycogen Liver © 2013 Pearson Education, Inc. Stimulates glycogen breakdown Glucagon
Factors That Influence Insulin Release • Elevated blood glucose levels – primary stimulus • Rising blood levels of amino acids and fatty acids • Release of acetylcholine by parasympathetic nerve fibers • Hormones glucagon, epinephrine, growth hormone, thyroxine, glucocorticoids • Somatostatin; sympathetic nervous system © 2013 Pearson Education, Inc.
Homeostatic Imbalances of Insulin • Diabetes mellitus (DM) – Due to hyposecretion (type 1) or hypoactivity (type 2) of insulin – Blood glucose levels remain high nausea higher blood glucose levels (fight or flight response) – Glycosuria – glucose spilled into urine – Fats used for cellular fuel lipidemia; if severe ketones (ketone bodies) from fatty acid metabolism ketonuria and ketoacidosis – Untreated ketoacidosis hyperpnea; disrupted heart activity and O 2 transport; depression of nervous system coma and death possible © 2013 Pearson Education, Inc.
Diabetes Mellitus: Signs • Three cardinal signs of DM – Polyuria—huge urine output • Glucose acts as osmotic diuretic – Polydipsia—excessive thirst • From water loss due to polyuria – Polyphagia—excessive hunger and food consumption • Cells cannot take up glucose; are "starving" © 2013 Pearson Education, Inc.
Homeostatic Imbalances of Insulin • Hyperinsulinism: – Excessive insulin secretion – Causes hypoglycemia • Low blood glucose levels • Anxiety, nervousness, disorientation, unconsciousness, even death – Treated by sugar ingestion © 2013 Pearson Education, Inc.
Table 16. 4 Symptoms of Insulin Deficit (Diabetes Mellitus) © 2013 Pearson Education, Inc.
Ovaries and Placenta • Gonads produce steroid sex hormones – Same as those of adrenal cortex • Ovaries produce estrogens and progesterone – Estrogen • Maturation of reproductive organs • Appearance of secondary sexual characteristics • With progesterone, causes breast development and cyclic changes in uterine mucosa • Placenta secretes estrogens, progesterone, and human chorionic gonadotropin (h. CG) © 2013 Pearson Education, Inc.
Testes • Testes produce testosterone – Initiates maturation of male reproductive organs – Causes appearance of male secondary sexual characteristics and sex drive – Necessary for normal sperm production – Maintains reproductive organs in functional state © 2013 Pearson Education, Inc.
Other Hormone-producing Structures • Heart – Atrial natriuretic peptide (ANP) decreases blood Na+ concentration, therefore blood pressure and blood volume • Kidneys – Erythropoietin signals production of red blood cells – Renin initiates the renin-angiotensinaldosterone mechanism © 2013 Pearson Education, Inc.
Developmental Aspects • Hormone-producing glands arise from all three germ layers • Most endocrine organs operate well until old age • Exposure to pesticides, industrial chemicals, arsenic, dioxin, and soil and water pollutants disrupts hormone function • Sex hormones, thyroid hormone, and glucocorticoids are vulnerable to the effects of pollutants • Interference with glucocorticoids may help explain high cancer rates in certain areas © 2013 Pearson Education, Inc.
Developmental Aspects • Ovaries undergo significant changes with age and become unresponsive to gonadotropins; problems associated with estrogen deficiency occur • Testosterone also diminishes with age, but effect is not usually seen until very old age © 2013 Pearson Education, Inc.
Developmental Aspects • GH levels decline with age - accounts for muscle atrophy with age • TH declines with age, contributing to lower basal metabolic rates • PTH levels remain fairly constant with age, but lack of estrogen in older women makes them more vulnerable to bonedemineralizing effects of PTH © 2013 Pearson Education, Inc.
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