chapter 18: the endocrine system
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Chapter 18: The Endocrine System. BIO 211 Lecture Instructor: Dr. Gollwitzer. Today in class we will: Compare intercellular communication in the endocrine and nervous systems - PowerPoint PPT PresentationTRANSCRIPT
Chapter 18: The Endocrine System
BIO 211 LectureInstructor: Dr. Gollwitzer
1
• Today in class we will:– Compare intercellular communication in the
endocrine and nervous systems• Learn the differences and similarities in each system’s
function(s) and how they are important with regard to homeostasis in the body
– Talk about hormones• The 3 major structural classes and examples of each• The secretion, distribution, and elimination of hormones• The mechanisms that allow hormones to affect target
cells and organs– Identify the organs of the endocrine system• Learn the names of the hormones that each endocrine
organ produces 2
Intercellular Communication• Cellular activities in the body must be
coordinated to maintain homeostasis (a stable internal environment within the body)
• Homeostasis is the key to survival in an ever changing environment– Failure to maintain homeostasis eventually leads to
illness or death• Activities in the human body are coordinated
through intercellular communication (communication between cells)
3
Table 18-1 Mechanisms of Intercellular Communication
4
Endocrine System vs. Nervous SystemDifferences
• Endocrine system– Endocrine
communication• Via hormones• Thru circulatory system
– Affects target cells in other tissues/organs distant to tissue of origin
– Slow response, but lasts much longer
• Nervous System– Neural (synaptic)
communication• Via neurotransmitters• Across synaptic cleft
– Affects limited, specific area (post-synaptic)
– Fast response, short-term crisis management
5
Endocrine System vs. Nervous SystemSimilarities
• Both systems:– Share many chemical messengers– Use chemical messengers that must bind to
specific receptors on their target cells– Share the common goal of maintaining
homeostasis
6
Endocrine System• One of the body’s two
coordination/communication systems– Nervous system is the other
• Endocrine glands are ductless glands• Communicate with other cells/organs/
systems in the body through release of hormones
• Endocrine cells hormone (chemical messenger) interstitial fluid or circulatory system target cells effect(s)
7
Examples of Endocrine Control
• Growth and maturation• Sexual development (puberty)• Reproduction• Response to environmental stress 24
hours/day for a lifetime
8
Hormone Structure• Divided into 3 major groups based on
chemical structure– Amino acid derivatives– Peptide hormones• Produced as inactive prohormones; converted to
active hormones
– Lipid derivatives
9
Hormone Structure:Amino Acid Derivatives
• Small molecules structurally related to amino acids
• Derivatives of tyrosine– Thyroid hormones – T3, T4– Catecholamines – epinephrine and
norepinephrine, dopamine• Derivative of tryptophan– Melatonin
10
Figure 18–2 11
Hormone Structure:Peptide Hormones
• Chains of amino acids• Synthesized as prohormones– Inactive molecules converted to active
hormones before or after secretion• 2 Groups– Glycoproteins– Short polypeptides and small proteins
12
Figure 18–2 13
Glycoproteins
• More than 200 amino acids long, with carbohydrates
• Released by:– Anterior pituitary: LH, FSH, TSH– Reproductive organs: inhibin– Kidneys: erythropoietin
14
Short Polypeptides andSmall Proteins
• All other hormones secreted by:– Hypothalamus– Anterior pituitary– Posterior pituitary– Pancreas– Parathyroid gland– Thymus, heart, and digestive tract
15
Hormone Structure:Lipid Derivatives
• 2 Classes– Steroid hormones• Synthesized from cholesterol
– Eicosanoids• Synthesized from arachidonic acid
16
Figure 18–2 17
Steroid Hormones
• Produced by:– Male and female reproductive organs• Testes androgens (testosterone)• Ovaries estrogens and progestins (progesterone)
– Adrenal glands corticosteroids– Kidneys calcitrol
• Bound to transport proteins in plasma (albumins, globulins) so remain in circulation longer than peptide hormones
18
Eicosanoids
• Small molecules with 5-C ring at one end• Important local (paracrine) hormones secreted by
all cells except RBCs• Primarily affect neighboring cells– Coordinate cellular activities– Affect enzymatic processes in extracellular fluid
• 2 Types– Leukotrienes (from WBCs or leukocytes)
• Coordinate tissue response to injury or disease
– Protaglandins (produced by most tissues of the body)• Coordinate local cellular activities
19
Hormone Distribution and Transport
• Hormones secreted/released into:– Interstitial space– Capillaries
• Circulate/distributed through bloodstream as:– Free hormones– Bound hormones
20
Free Hormones• Proteins, polypeptides, amino acid
derivatives• Rapidly removed from bloodstream– Diffuse out of bloodstream and bind to
receptors on target cells– Absorbed by liver or kidney and broken down– Broken down by enzymes in plasma or
interstitial fluids• Functional for <1 hr
21
Bound Hormones• Thyroid and steroid hormones• Bound to transport proteins in blood, i.e.,
albumins and globulins• Remain in circulation much longer (weeks)
22
Hormone Function and Mechanism of Action on Target Organs
• Alter cellular operations• Change biochemical properties or physical
structure of target cells– Activate genes in nucleus that code for synthesis
of enzyme or structural protein– Turn existing enzyme on or off by changing its
shape or structure– Increase/decrease rate of synthesis of enzyme or
other protein
23
Hormone Function and Mechanism of Action
• Hormone effect depends on:– Type of target cell– Type of receptor = protein molecule to which
particular hormone binds strongly• Requires interaction of hormone with
appropriate receptor• Presence or absence of specific receptor
determines cell’s hormonal sensitivities– Receptor present response– Receptor absent no response
24
Hormone Receptors
• On cell membrane (extracellular)– For water-soluble hormones (can’t cross
membrane)• Catecholamines (E and NE)• Peptide hormones
– Hormones can’t have direct effect inside cell– Act as first-messenger • Causes second-messenger to appear in cytoplasm
(cAMP, cGMP, Ca++)• Second messenger changes in rates of metabolic
reactions
25
Figure 18–3
26
Hormone Receptors• Inside cell (intracellular)– For lipid-soluble hormones (can cross membrane)
• Steroid and thyroid hormones
– Cross cell membrane and bind to receptors in cytoplasm or nucleus
– Hormone/receptor complex activates/inactivates specific genes and changes protein/enzyme synthesis, e.g., • Testosterone stimulates production of enzymes and protein in
skeletal muscle, causing increased muscle mass and strength• Thyroid hormones increase/decrease concentrations of enzymes
and bind to mitochondria and increase ATP production
27
Figure 18–4 28
Endocrine Organs• Hypothalamus• Pituitary gland• Thyroid gland• Parathyroid glands• Adrenal glands• Pineal gland• Pancreas• Kidneys• Other: heart, thymus, adipose tissue• Reproductive organs (gonads and placenta)
29
Fig 18-1
30
• Today in class we will:– Discuss the hormones (and each hormone’s function)
along with the general effects of abnormal levels of each hormone produced by the:• Hypothalamus
– More in depth info on the hypothalamus:» The structural relationship of the hypothalamus and pituitary
gland» Learn about the hypophyseal portal system and its
importance» Learn how the hypothalamus controls endocrine function
• Pituitary gland» Identify hormones secreted by the posterior pituitary gland
and produced and secreted by the anterior pituitary gland• Thyroid gland • Parathyroid glands
31
Hypothalamus:A Neuroendocrine Organ
• Neural effects – Controls feeding reflexes, heart rate, blood pressure,
body temp, day-night activity cycles
• Endocrine contribution– Hormone synthesis (for release by posterior pituitary),
i.e., ADH and OT• Transported via axons of neurosecretory cells to posterior
pituitary for release
– Hormone synthesis and release, i.e., RHs• Transported via hypophyseal portal system to anterior
pituitary
32
Figure 14–10a
Hypothalamus
33
Hypothalamic Hormones
• Hypothalamus produces:– ADH (antidiuretic hormone)– OT (oxytocin)– RHs (regulatory hormones)
34
Hypothalamic Hormones
• ADH (antidiuretic hormone)– Produced by supraoptic nuclei (released by
posterior pituitary)– Effects• Decreases water lost at kidneys by increasing
reabsorption• Elevates blood pressure through vasoconstriction
– Release inhibited by alcohol why you urinate a lot while drinking
35
Diabetes Insipidus
• Inadequate amounts of ADH released from posterior pituitary
• Impairs water conservation at kidneys watery urine
36
Hypothalamic Hormones
• OT (oxytocin)– Produced by paraventricular nuclei (released by
posterior pituitary)– Produced during:• Sex, breastfeeding, and other bonding experiences
(increases trust and compassion)• Labor
– Stimulates smooth muscle in:• Mammary gland milk ejection• Uterus to promote labor and delivery• Male and female reproductive tracts
– Plays a role in sexual function37
Hypothalamic Hormones
• RHs (regulatory hormones)– Produced by median eminence (tuberal area)– Stimulate/inhibit anterior pituitary hormone
synthesis and release
38
Hypophyseal Portal System
• Prevents dilution of very small quantities of RHs by systemic circulation
• Ensures RHs entering portal vessels will reach target cells in anterior pituitary
39
Fig 18-740
Control of Endocrine Organs
• Involves endocrine reflexes, i.e., stimulus hormone secretion
• In most cases, controlled by negative feedback mechanisms
• Hormones released in response to one or more of the following stimuli:– Humoral– Neural– Hormonal
41
Control of Endocrine Organs
• Humoral stimuli– From local changes in composition of
extracellular fluid– Hormones released continually, but rate rises and
falls in response to humoral stimulation• e.g., pancreatic hormones
increased blood glucose increased extracellular glucose increased insulin
42
Control of Endocrine Organs
• Neural stimuli– Via arrival of neurotransmitters at neuroglandular
junctions• e.g., hypothalamic control of adrenal medullae via
action potentials along efferent nerve fibers (also have hormonal component)– Hypothalamus has autonomic centers that exert direct neural
control over endocrine cells of adrenal medullae– When sympathetic division activated, adrenal medullae
release E and NE into bloodstream
43
Control of Endocrine Organs
• Hormonal stimuli– Via arrival/removal of hormones from other
endocrine glands• Hypothalamus
– Highest level of endocrine control– Secretes regulatory hormones/factors that stimulate
synthesis and secretion of anterior pituitary hormones and/or prevent the synthesis and secretion of hormones
• Anterior pituitary – Hormones it secretes controls activities of other endocrine
organs (thyroid, adrenal cortex, reproductive organs)
44
Hypothalamic Control ofEndocrine Function
• Involves most complex responses• Integrates activities of nervous and
endocrine systems• 3 mechanisms– Secretion of AP regulatory hormones– Production of ADH and oxytocin– Control of sympathetic stimulation of adrenal
medullae
45
Figure 18–5 46
Hypothalamic Control ofEndocrine Function
• Secretion of AP regulatory hormones– Neurosecretory cells in median eminence of Hth
secrete RHs– Delivered to AP thru hypophyseal portal system– Control release of AP hormones (e.g., TSH, ACTH,
FSH, LH) that control other endocrine organs– Rate of RH release controlled by negative
feedback
47
Hypothalamic Regulatory Hormones
Figure 18–8a48
Hypothalamic Control ofEndocrine Function
• Production of ADH and oxytocin– Hth acts as endocrine organ by producing ADH
and oxytocin that are released by PP– Neurosecretory cells connect Hth to PP– ADH and oxytocin packaged in vesicles and
transported along axons to PP where they are stored in axon terminals
– When neurosecretory cells stimulated, action potential triggers release of stored ADH and oxytocin from PP
49
Hypothalamic Control ofEndocrine Function
• Control of sympathetic stimulation of adrenal medullae– Hth contains autonomic centers– Exert direct control over adrenal medullae E
and NE
50
Pituitary Gland (Hypophysis)
Figure 18–6
51
Pituitary Gland (Hypophysis)
• Releases 9 important peptide hormones– 2 from posterior pituitary (produced in
hypothalamus)– 7 from anterior pituitary (produced in anterior
pituitary)• Peptide hormones:– Bind to membrane receptors– Use a second messenger (cAMP)
52
Hypothalamic/Posterior Pituitary Hormones
• ADH (antidiuretic hormone)– Produced by supraoptic nuclei– Released from axons of neurosecretory cells
• Oxytocin– Produced by paraventricular nuclei– Released from axons of neurosecretory cells
(See earlier discussion of hypothalamic hormones.)
53
Anterior Pituitary Gland Hormones
Anatomy and Physiology is
Tough
Going
For
Many
Learners
= ACTH/adrenocorticotropic hormone= PRL/prolactin= TSH/thyroid-stimulating hormone
= GH/growth hormone= FSH/follicle-stimulating hormone
= MSH/melanocyte-stimulating hormone
= LH/luteinizing hormone
Mnemonic:Anatomy and physiology is tough going for many learners.
54
Pituitary Gland Hormones
Fig 18-9
55
Anterior Pituitary Hormones
• ACTH (adrenocorticotropic hormone)– Stimulates release of steroid hormones
(glucocorticoids) by adrenal cortex• TSH (thyroid-stimulating hormone)– Stimulates secretion of thyroid hormones
• PRL (prolactin)– “Social bonding” hormone; increases with social
interaction, touch– Stimulates development of mammary glands and
milk production56
Anterior Pituitary Hormones• GH (growth hormone or somatotropin)– Stimulates release of somatomedins (peptide
hormones) from liver cells• Accelerate protein synthesis and cell growth, esp.
skeletal muscle and cartilage– Stimulates cell division– Metabolic effects• Glucose-sparing effect
– Stimulates adipocytes: triglycerides (TGs) fatty acids (FA) ATP (vs. glu ATP)
• Diabetogenic effect– Stimulates liver: glycogen glucose
57
Anterior Pituitary Hormones• MSH (melanocyte-stimulating hormone)– Stimulates melanocytes in stratum germinativum of skin
(Fig 5-5) melanin (brown, black or yellow-brown pigment)
– Not normally secreted by nonpregnant adult humans– Secreted during:
• Fetal development• Early childhood• Pregnancy• Certain diseases
– In nonhuman vertebrates seasonal change in hair coat color
58
Anterior Pituitary Hormones
• Gonadotropins– Follicle-stimulating hormone (FSH)– Luteinizing hormone (LH)
• Regulate activities of gonads (testes, ovaries)• Stimulates release of steroid hormones by
gonads, e.g., estrogens, progestins, androgens
59
Anterior Pituitary Hormones
• Follicle-stimulating hormone (FSH)– In females• Stimulates follicle development and estrogen secretion• Promotes oocyte development
– In males• Stimulates sustentacular cells• Promotes sperm development
– Production inhibited by inhibin (peptide hormone)
60
Anterior Pituitary Hormones
• Luteinizing hormone (LH)– In females• Causes ovulation and progesterone production by
corpus luteum (CL)
– In males (aka interstitial cell-stimulating hormone, ICSH)• Causes androgen production by interstitial cells of
testes
61
Thyroid Gland
Fig 18-10a 62
Thyroid Gland Hormones
• Follicle cells– Simple cuboidal epithelium– Synthesize and release “thyroid hormones”• T3 (triiodothyronine)• T4 (tetraiodothyronine)
• C (clear, parafollicular) cells – Synthesize and release calcitonin
63
Fig 18-10c 64
Fig 18-11a 65
Fig 18-11b 66
Effects of Thyroid Hormones• Many, diverse effects• On almost every cell in the body– Especially metabolically active tissues and organs, e.g.,
skeletal muscle, liver, kidneys• Increase– Cellular metabolism, e.g., energy utilization, oxygen
consumption– RBC formation– Growth and development– Heart rate, contraction– Mineral turnover in bone
• Calorigenic/thermiogenic effect– Enables body to adapt to cold temperatures
67
Hypothyroidism• Inadequate production of thyroid hormones– From inadequate dietary iodide
• Effects– In later childhood: retarded growth and mental
development; delayed puberty– In adults: lethargy, unable to tolerate cold temperatures,
leads to myxedema (subcutaneous swelling, dry skin, hair loss, low body temp, muscular weakness, slowed reflexes)
– Most commonly diagnosed in women >50 y.o.• Congenital– Cretinism (in an infant); inadequate skeletal and nervous
development; metabolic rate dec 40%
68
69
Hyperthyroidism• Excessive quantities of thyroid hormones;
thyrotoxicosis (“poisoning”)• Effects– Increased metabolic rate, increased blood pressure and
heart rate, irregular heart beat, skin flushed and moist with perspiration
– Restless, excitable, subject to shifts in moods and emotional states
– Limited energy reserves and fatigues easily• Graves’ Disease– May be accompanied by exophthalmia or goiter– Common with age (affected both George Bush Sr. and
Barbara Bush)
70
71
C Cell Hormone Production• C cells (interspersed between follicles)– Respond to increased calcium levels– Produce calcitonin
• Effects of calcitonin– Decreases calcium levels in body fluids (“tones down” Ca)
• Increases calcium excretion at kidneys• Inhibits osteoclast activity
– Especially impt during childhood (stimulates bone growth) and pregnancy (when maternal skeleton competes with developing fetus for Ca++)
– Opposes action of parathyroid hormone (PTH) which increases calcium
72
Calcitonin
Figure 6–16b73
Parathyroid Glands
Fig 18-12a 74
Parathyroid Glands• Principal (chief) cells– Respond to decreased calcium levels– Produce PTH (parathyroid hormone)
• PTH– Increases calcium levels in body fluids• Decreases calcium excretion at kidneys• Stimulates osteoclasts• Increases intestinal absorption of calcium (with
calcitriol)– Opposes action of calcitonin (from thyroid) which
decreases calcium– Primary regulator of blood calcium in adults
75
Parathyroid Hormone (PTH)
Figure 6–16a76
Hypoparathyroidism
• Inadequate PTH production• Low calcium levels in body fluids• Nervous system more excitable; may lead to
muscle tetany (prolonged muscle spasms that initially involve limbs and face)
77
Hyperparathyroidism
• Abnormally high PTH levels• High calcium levels in body fluids• CNS function depressed• Thin, brittle bones; weak skeletal muscles• Nausea, vomiting• May become comatose
78
Functions of Calcium
• Calcium especially important to– Membranes– Neurons (conduction)– Muscle cells (contraction; especially cardiac)
• Must be closely regulated
79
Review of Calcium Homeostasis• Regulated by 2 major hormones– Calcitonin– PTH
• Hormones affect:– Ca excretion (kidneys)– Ca storage (bones)– Ca absorption (digestive tract)
• Calcium homeostasis– ↑Ca ↑Calcitonin ↓Ca– ↓Ca ↑PTH ↑Ca
80
Fig 18-13 81
• Today in class we will:– Continue our discussion of the hormones (and each
hormone’s function) along with the general effects of abnormal levels of each hormone produced by the:• Adrenal glands
– Identify the region of the adrenal gland in which each adrenal hormone is produced
• Pineal gland• Pancreas• Gastrointestinal tract• Kidneys• Heart• Thymus• Gonads• Adipose tissue
82
• Today in class we will:– Describe the:• 4 possible outcomes to exposure to multiple hormones• Role of hormones in growth• Hormonal responses to stress
– The 4 possible outcomes when cells are exposed to multiple hormones
– Examples of complex hormone interactions– The role of hormones in the growth process– Hormonal responses to stress– Interactions between the endocrine system and
other body systems
83
Adrenal Glands
Fig 18-14a 84
Adrenal Glands• aka Suprarenal glands• Location– On superior surface of kidneys
• 2 regions– Adrenal cortex• steroid hormones (adrenocortical steroids/
corticosteroids)– Adrenal medulla• epinephrine and norepinephrine (E, NE)• Under ANS control)
85
Fig 18-14b86
Adrenal Cortex: Zona Glomerulosa
• Produces mineralocorticoids, primarily aldosterone• Effects: primarily on electrolytes– Increases renal (kidney) reabsorption of sodium (and
water)– Increases urinary loss of potassium
• Stimulated by:– Decreased plasma sodium levels– Increased plasma potassium levels– Decreased blood volume or BP– Angiotensin II
• Inhibited by natriuretic peptides (e.g. atrial natriuretic peptide, ANP)
87
Adrenal Cortex: Zona Fasciculata
• Produces glucocorticoids (cortisol/cortisone, hydro-cortisone)
• Effects– Glucose-sparing
• In liver-forms glucose and stimulates gluglycogen• In muscle-releases amino acids for gluconeogenesis (aaglu)• In adipose tissues-releases lipids for gluconeogenesis; promotes
lipid utilization (like GH)
– Anti-inflammatory• Inhibits activity of WBCs (cortisone used for poison ivy, insect
bites)
• Stimulated by ACTH
88
Adrenal Cortex: Zona Reticularis• Produces androgens (converted to estrogens)• Effects – Not important in adult men– Promotes bone growth, muscle growth, and blood
formation in women and children• Stimulated by ACTH
89
Adrenal Medullae• Secretes epinephrine and norepinephrine• E and NE secreted– Continuously at low levels via exocytosis– During ANS sympathetic activation
• Effects– Mobilize energy stores• Glycogen in skeletal muscle and liver glucose
increased muscular strength and endurance– Accelerate energy utilization• breakdown of glucose and fats ATP
– Increase heart rate and contraction90
Figure 14–11a
Pineal Gland
91
Pineal Gland• Has neuroendocrine (neural and endocrine) effects
(like hypothalamus)• Pinealocytes produce melatonin– Time-keeping hormone; released in brain in response to
darkness and tells body it’s time for sleep– Establishes circadian rhythms = daily changes in
physiological processes that follow regular pattern (e.g., body temperature, hormone and enzyme levels)
– Inhibits reproductive function, e.g., maturation of sperm, oocytes, reproductive organs; decreases at puberty
– An antioxidant; may protect CNS neurons from free radicals (NO, H2O2) generated in active neural tissue
– Inhibits MSH (secreted by anterior pituitary)
92
Figure 18–15
Pancreas
93
Pancreas• Exocrine– Clusters of gland cells (pancreatic acini and
ducts)– Release enzyme-rich fluid for digestion into small
intestine• Endocrine– Regulates blood glucose concentrations– 2 major cell types: alpha and beta cells
94
Pancreas• Alpha cells– Secrete glucagon• Released in response to decreased blood glucose levels• Increase blood glucose levels via:
– Glycogen breakdown glucose (skeletal muscle and liver)– Fats FAs glucose (adipose tissue)– Glucose manufacture (liver)
95
Pancreas• Beta cells– Secrete insulin• Released in response to increased blood glucose• Receptors present in most cell membranes
– Except brain, kidneys, digestive tract epithelium, RBCs (insulin-independent)
• Decreases blood glucose levels– Increases glucose uptake and utilization by most cells– Increases glycogen synthesis from glucose in skeletal muscle
and liver
• Stimulates amino acid absorption and protein synthesis• Stimulates triglyceride formation in adipose tissue
96
Pancreatic Islets
Figure 18–1697
Review of Glucose Homeostasis
• Increased blood glucose beta cells increase insulin secretion decreased blood glucose
• Decreased blood glucose alpha cells increase glucagon secretion increased blood glucose
98
Diabetes Mellitus• Occurs when glucose concentration so high it
overwhelms normal reabsorption capabilities of kidneys– Glycosuria and polyuria
• Caused by:– Genetic abnormalities (inadequate insulin production,
abnormal insulin, defective receptor proteins)– Pathological conditions– Injuries– Immune disorders– Hormonal imbalances– Obesity
99
Diabetes Mellitus• Two major types– Type I
• Insulin-dependent, juvenile-onset• May be autoimmune disease• Occurs first in childhood or young-adulthood• Body does not produce insulin, so must take daily insulin for
rest of life– Type II
• Non insulin-dependent, adult-onset• Develops gradually• Most often in people over 45, but seen younger (even
children) with increasing obesity problems• Accounts for 90-95% of diabetes in US• Body doesn’t make enough insulin or doesn’t use insulin
effectively100
Diabetes Mellitus
• Symptoms– Extreme fatigue– Excessive thirst– Frequent urination– Extreme hunger– Weight loss– Irritability– Blurred vision– Vaginal yeast infections
• Chronic Medical Problems– Retinopathy, cataracts– Nephropathy– Neuropathy– Degenerative changes in
cardiac circulationTIAs and early heart attacks
– Reduced blood flow to limbs; extreme cases require amputation
101
Gastrointestinal (GI) Tract
• All coordinate digestive activities ( Function):– Secretin– Gastrin– CholecystokininNOTE: There are many hormones associated with the digestive system.
These are just a few examples.
• Primary targets are other regions and organs of the digestive system
102
Figure 26–2
Kidneys
103
Kidneys• Hormones produced– Erythropoietin (EPO)• Stimulates RBC production by bone marrow• Secreted when oxygen is low (hypoxia) due to
– Disease– High altitude
– Calcitriol• UV radiation epidermal cells cholecalciferol (vit
D3) liver (intermediary product) kidneys calcitriol• Stimulates calcium and phosphate ion absorption
along the digestive tract104
Calcitriol
Figure 18–17a105
Kidneys• Enzyme produced = renin– Converts prohormone angiotensinogen to hormone
angiotensin I (in liver) (“tenses blood vessels”)– Angiotensin I converted to hormone angiotensin II (in lung
capillaries)– Angiotensin II
• Stimulates adrenal aldosterone increased blood Na and volume (blood pressure, BP)
• Stimulates posterior pituitary ADH (produced by supraoptic nucleus of hypothalamus) increased blood volume (BP)
• Stimulates thirst increased blood volume (BP) • Constricts blood vessels increased BP
106
The Renin–Angiotensin System
Figure 18–17b 107
Heart
• When blood volume high, cardiac muscle cells produce natriuretic peptides (NPs)– ANP = atrial NP– BNP = brain NP (produced by ventricles)
• Natriuretic peptides– Act opposite to angiotensin II– Reduce blood volume and blood pressure
108
Thymus
• Produces thymosin hormones– Help develop and maintain normal immune
defenses (T cell development)
109
Gonads • Testes– Interstitial cells androgens• Testosterone is most important
– Sustentacular cells inhibin• Supports sperm development
• Ovaries– Follicle cells produce estrogens• Primarily estradiol
– After ovulation, follicle cells:• Reorganize into corpus luteum (CL)• Release estrogens and progestins, primarily progesterone
110
Adipose Tissue Secretions
• Leptin– Inhibits appetite
111
Endocrine Disorders• GH– Excess production • Gigantism - before epiphyseal plates close• Acromegaly - after epiphyseal plates close
– Under-production • Pituitary growth failure (dwarfism)
• ADH– Inadequate productiondiabetes insipidus
(polyuria)
112
Endocrine Disorders• Thyroid Gland– Hypothyroidism• Cretinism• Goiter
– Hyperthyroidism• Graves Disease (exophthalmia)
• Adrenal– Inadequate GC production • Addison’s Disease - inadequate GC production
– Excess GCs Cushing’s Disease (due to hypersecretion of ACTH)
113
114
Patterns of Hormonal Interaction• Cells never respond to only one hormone; respond to
multiple hormones simultaneously• When cell receives instructions from 2 hormones at once
4 possible effects:– Antagonistic (opposing): result depends on balance between two
hormones, e.g., insulin and glucagon, PTH and calcitonin)– Synergistic (additive): both hormones give same instructions and
effect is magnified, e.g., GH and glucocorticoids glucose-sparing effect
– Permissive: first hormone needed for second hormone to produce effect, e.g., thyroid hormones must be present for epinephrine effect on energy consumption
– Integrative (different but complementary results): important in coordinating activities of different physiological systems, e.g., calcitriol and PTH effects on tissues involved in calcium metabolism
115
Examples of Complex Hormone Interactions
• Growth– Involves GH, thyroid hormones, insulin, PTH,
calcitriol, reproductive hormones
• Behavior– Many hormones involved– Produce changes in mood, emotional states
and behavior
116
Examples of Complex Hormone Interactions
• Stress– General Adaptation Syndrome (GAS) or stress
response– Divided into 3 phases• Alarm phase• Resistance phase• Exhaustion phase
117
Figure 18–18118
General Adaptation Syndrome
• Alarm phase– Immediate response– Directed by sympathetic division of ANS– Epinephrine is dominant hormone– Energy reserves (glucose) mobilized from
glycogen– “Fight or flight” responses
119
General Adaptation Syndrome
• Resistance phase– Entered if stress lasts longer than few hours– Energy demands still high• Glycogen reserves nearly exhausted after hours of
stress– Glucocorticoids are dominant hormones• Mobilize lipid and protein reserves• Raise and stabilize blood glucose concentrations• Conserve glucose for neural tissues
120
General Adaptation Syndrome
• Exhaustion phase– Begins when homeostatic regulation breaks
down– Failure of 1 or more organ systems proves fatal
121
Interactions between Endocrine and Other Systems
Figure 18–19 122