prepared by Human Anatomy & Physiology Barbara Heard ...10/26/2014 5 © 2013 Pearson Education, Inc. Figure 16.5b The hypothalamus controls release of hormones from the pituitary gland

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Human Anatomy & PhysiologyNinth Edition

PowerPoint® Lecture Slides

prepared by

Barbara Heard,

Atlantic Cape Community

College

© 2013 Pearson Education, Inc.© Annie Leibovitz/Contact Press Images

C H A P T E R 16

The Endocrine

System: Part A

© 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



• 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



• Exocrine glands

– Nonhormonal substances (sweat, saliva)

– Have ducts to carry secretion to membrane

surface

• Endocrine glands

– Produce hormones

– Lack ducts



• 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


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

• Testis (male)

• Ovary (female)

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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


Chemistry of Hormones

• Two main classes

– Amino acid-based hormones

• Amino acid derivatives, peptides, and proteins

– Steroids

• Synthesized from cholesterol

• Gonadal and adrenocortical hormones


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)

• 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)

• Act on intracellular receptors that directly activate

genes

• Can enter cell


Slide 1Figure 16.2 Cyclic AMP second-messenger mechanism of water-soluble hormones.

Recall from Chapter 3 that

G protein signaling mechanisms

are like a molecular relay race.

Hormone

(1st messenger)

Receptor G protein Enzyme 2nd

messenger

Adenylate cyclase Extracellular fluid

G protein (Gs)

GDP

Receptor

Hormone (1st messenger)

binds receptor.

Receptor

activates G

protein (Gs).

G protein

activates

adenylate

cyclase.

Adenylate

cyclase converts

ATP to cAMP (2nd

messenger).

Inactive

protein

kinase

Triggers responses of

target cell (activates

enzymes, stimulates

cellular secretion,

opens ion channel, etc.)

Active

protein

kinase

cAMP activates

protein kinases.

Cytoplasm

cAMP

GTP

GTP

GTP

ATP

1

2 3 4

5


Figure 16.3 Direct gene activation mechanism of lipid-soluble hormones. Slide 1

The steroid hormone

diffuses through the plasma

membrane and binds an

intracellular receptor.

1

5

The receptor-hormone complex enters the nucleus.

The receptor- hormone complex binds a specific DNA region.

Binding initiates transcription of the gene to mRNA.

The mRNA directs protein synthesis.

New protein

Nucleus

mRNA

DNA

ReceptorBinding region

Receptor-hormonecomplex

Receptor

protein

Steroidhormone Plasma

membrane

Extracellularfluid

Cytoplasm

2

3

4

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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


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


Figure 16.4a Three types of endocrine gland stimuli. Slide 1

Humoral Stimulus

Hormone release caused by altered

levels of certain critical ions or

nutrients.

Stimulus: Low concentration of Ca2+ in

capillary blood.

Parathyroidglands

Parathyroidglands

Capillary (low Ca2+

in blood)

Thyroid gland(posterior view)

PTH

Response: Parathyroid glands secrete

parathyroid hormone (PTH), whichincreases blood Ca2+.


Neural Stimuli

• Nerve fibers stimulate hormone release

– Sympathetic nervous system fibers stimulate

adrenal medulla to secrete catecholamines


Figure 16.4b Three types of endocrine gland stimuli. Slide 1

Neural Stimulus

Hormone release caused

by neural input.

Stimulus: Action potentials in preganglionicsympathetic fibers to adrenal medulla.

CNS (spinal cord)

Preganglionicsympatheticfibers

Medulla ofadrenal gland

Capillary

Response: Adrenal medulla cells secreteepinephrine and norepinephrine.


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

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Figure 16.4c Three types of endocrine gland stimuli. Slide 1

Hormonal Stimulus

Hormone release caused by another

hormone (a tropic hormone).

Stimulus: Hormones from hypothalamus.

Anteriorpituitarygland

Thyroidgland

Adrenalcortex

Gonad(Testis)

Hypothalamus

Response: Anterior pituitary gland secreteshormones that stimulate other endocrine glands to secrete hormones.


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


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


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


The Pituitary Gland and Hypothalamus

• Pituitary gland (hypophysis) has two

major lobes

–Posterior pituitary (lobe)

• Neural tissue

–Anterior pituitary (lobe)

(adenohypophysis)

• Glandular tissue


Figure 16.5a The hypothalamus controls release of hormones from the pituitary gland in two different ways (1 of 2).

Slide 1

Hypothalamic neurons synthesize oxytocin or antidiuretic hormone (ADH).

Oxytocin and ADH are stored in axon terminals in the posterior pituitary.

When hypothalamic neurons fire, action potentials arriving at the axon terminals cause oxytocin or ADH to be released into the blood.

1

2

3

4OxytocinADH

Posterior lobe

of pituitary

Opticchiasma

Infundibulum(connecting stalk)

Hypothalamic-hypophyseal

tract

Axon terminals

Posterior lobe

of pituitary

Paraventricular nucleus

Hypothalamus

Supraopticnucleus

Inferiorhypophysealartery

Oxytocin and ADH are transported down the axons of the hypothalamic- hypophyseal tract to the posterior pituitary.

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Figure 16.5b The hypothalamus controls release of hormones from the pituitary gland in two different ways (2 of 2).

Slide 1

Hypothalamic hormones travel through portal veins to the anterior pituitary where they stimulate or inhibit release of hormones made in the anterior pituitary.

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

When appropriately stimulated, hypothalamic neurons secrete releasing or inhibiting hormones into the primary capillary plexus.

Hypophyseal

portal system

• Primary capillaryplexus

• Hypophysealportal veins

• Secondarycapillary plexus

Superiorhypophyseal

artery

Anterior lobe

of pituitary

Hypothalamus Hypothalamicneurons synthesizeGHRH, GHIH, TRH,CRH, GnRH, PIH.

A portal system is two capillary plexuses (beds) connected by veins.

1

2

3


Posterior Pituitary and Hypothalamic

Hormones

• Oxytocin and ADH

– Each composed of nine amino acids

– Almost identical – differ in two amino acids


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


Anterior Pituitary Hormones

• Growth hormone (GH)

• Thyroid-stimulating hormone (TSH) or

thyrotropin

• Adrenocorticotropic hormone (ACTH)

• Follicle-stimulating hormone (FSH)

• Luteinizing hormone (LH)

• Prolactin (PRL)


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)


Homeostatic Imbalances of Growth

Hormone

• Hypersecretion

– In children results in gigantism

– In adults results in acromegaly

• Hyposecretion

– In children results in pituitary dwarfism

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Figure 16.6 Growth-promoting and metabolic actions of growth hormone (GH).

Hypothalamus

secretes growth

hormone–releasing

hormone (GHRH), and

GHIH (somatostatin)Anterior

pituitary

Inhibits GHRH release

Stimulates GHIH release

Inhibits GH synthesis

and release

Feedback

Indirect actions

(growth-

promoting)

Liver and

other tissues

Insulin-like growth

factors (IGFs)

Produce

Effects

Skeletal ExtraskeletalFat

metabolism

Carbohydrate

metabolism

Direct actions

(metabolic,

anti-insulin)

Effects

Growth hormone (GH)

Increased cartilage

formation and

skeletal growth

Increased protein

synthesis, and

cell growth and

proliferation

Increased

fat breakdown

and release

Increased blood

glucose and other

anti-insulin effects

Increases, stimulates

Initial stimulus

Reduces, inhibits

Physiological response

Result


Figure 16.7 Disorders of pituitary growth hormone.


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


Hypothalamus

TRH

Anterior pituitary

TSH

Thyroid gland

Thyroidhormones

Target cellsStimulates

Figure 16.8 Regulation of thyroid hormone secretion.

Inhibits


Adrenocorticotropic Hormone

(Corticotropin)

• Regulation of ACTH release

– Triggered by hypothalamic corticotropin-

releasing hormone (CRH) in daily rhythm

– Internal and external factors such as fever,

hypoglycemia, and stressors can alter release

of CRH


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

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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


Thyroid Hormone (TH)

• Actually two related compounds

– T4 (thyroxine); has 2 tyrosine molecules + 4

bound iodine atoms

– T3 (triiodothyronine); has 2 tyrosines + 3

bound iodine atoms

• Affects virtually every cell in body


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


Figure 16.10 Synthesis of thyroid hormone. Slide 1

Thyroglobulin is synthesized and discharged into the follicle lumen.

1

2

3

4

5

6

7

Golgi

apparatus

Iodide (I−)

Rough

ER

Capillary

Iodide (I–) is trapped (actively transported in).

Lysosome

Lysosomal enzymes cleave T4 and T3 from thyroglobulin and hormones diffuse into bloodstream.

Thyroglobulin colloid is endocytosed and combined with a lysosome.

Iodinated tyrosines are linked together to form T3

and T4.

Iodide is oxidized to iodine.

Iodine is attached to tyrosine in colloid, forming DIT and MIT.

To peripheral tissues

Colloid in

lumen of

follicle

Thyroid follicular cells

Tyrosines (part of thyroglobulin

molecule)

Thyro-

globulin

colloid

T3

T4

T3

T4

T3

T4

Iodine

DIT MIT

Colloid


Transport and Regulation of TH

• T4 and T3 transported by thyroxine-binding

globulins (TBGs)

• Both bind to target receptors, but T3 is ten

times more active than T4

• Peripheral tissues convert T4 to T3


Hypothalamus

TRH

Anterior pituitary

TSH

Thyroid gland

Thyroidhormones

Target cellsStimulates

Figure 16.8 Regulation of thyroid hormone secretion.

Inhibits

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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


Figure 16.11 Thyroid disorders.


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 Ca2+

from bone matrix

– Stimulates Ca2+ uptake and incorporation into

bone matrix


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 Ca2+

homeostasis


Figure 16.12 The parathyroid glands.

Parathyroid

glands

Parathyroid

cells

(secrete

parathyroid

hormone)

Capillary

Oxyphil

cells

Pharynx

(posterior

aspect)

Thyroid

gland

Esophagus

Trachea


Figure 16.13 Effects of parathyroid hormone on bone, the kidneys, and the intestine.

Osteoclast activity

in bone causes Ca2+

and PO43- release

into blood

Hypocalcemia

(low blood Ca2+

)

PTH release from

parathyroid gland

Ca2+ reabsorption

in kidney tubule

Activation of

vitamin D by kidney

Ca2+ absorptionfrom food in small

intestine

Ca2+ in blood

Initial stimulus

Physiological response

Result

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Homeostatic Imbalances of PTH

• Hyperparathyroidism due to tumor

– Bones soften and deform

– Elevated Ca2+ 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


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


Figure 16.14 Microscopic structure of the adrenal gland.

Me

du

lla

Co

rte

x

Capsule

Zona

glomerulosa

Zona

fasciculata

Zona

reticularis

Adrenal

medulla

Adrenal gland

• Medulla

• Cortex

Kidney

Hormones

secreted

Aldosterone

Cortisolandandrogens

Epinephrineandnorepinephrine

Photomicrograph (115x)Drawing of the histology of the

adrenal cortex and a portion of

the adrenal medulla


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


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


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

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Figure 16.16 The effects of excess glucocorticoid.

Patient before onset. Same patient with Cushing's

syndrome. The white arrow showsthe characteristic "buffalo hump" offat on the upper back. © 2013 Pearson Education, Inc.

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


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


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


Adrenal Medulla

• Hypersecretion

– Hyperglycemia, increased metabolic rate,

rapid heartbeat and palpitations,

hypertension, intense nervousness, sweating

• Hyposecretion

– Not problematic

– Adrenal catecholamines not essential to life


Figure 16.17 Stress and the adrenal gland.

Short-term stress Prolonged stress

Nerve impulses

Spinal cord

Preganglionic

sympathetic

fibers

Adrenal medulla

(secretes amino acid–

based hormones)

Catecholamines

(epinephrine and

norepinephrine)

Short-term stress response

Stress

Hypothalamus

Corticotropic cells

of anterior pituitary

To target in blood

CRH (corticotropin-

releasing hormone)

Adrenal cortex

(secretes steroid

hormones)

Mineralocorticoids Glucocorticoids

ACTH

• Heart rate increases

Long-term stress response

• Kidneys retain

sodium and water• Proteins and fats converted

to glucose or broken down

for energy• Blood glucose 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

• Blood volume and

blood pressure

rise • Immune system

supressed

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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


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)


Figure 16.18 Photomicrograph of differentially stained pancreatic tissue.

Pancreatic islet

• (Glucagon-producing) cells

• (Insulin-producing) cells

Pancreatic acinar

cells (exocrine)


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


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


Figure 16.19 Insulin and glucagon from the pancreas regulate blood glucose levels.

Stimulates glucose

uptake by cells

Insulin

Stimulates

glycogen

formationwPancreas

Tissue cells

Glucose Glycogen

Liver

Blood

glucose

falls to

normal

range.

Stimulus

Blood

glucose level

Pancreas

Glucose Glycogen

Liver Stimulates

glycogen

breakdown

Bloodglucoserises tonormalrange.

Stimulus

Blood

glucose level

Glucagon

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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


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 O2 transport; depression of nervous

system coma and death possible


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"


Homeostatic Imbalances of Insulin

• Hyperinsulinism:

– Excessive insulin secretion

– Causes hypoglycemia

• Low blood glucose levels

• Anxiety, nervousness, disorientation,

unconsciousness, even death

– Treated by sugar ingestion


Table 16.4 Symptoms of Insulin Deficit (Diabetes Mellitus)


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 (hCG)

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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


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-angiotensin-

aldosterone mechanism


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



• 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



• 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 bone-

demineralizing effects of PTH

Documents

prepared by Human Anatomy & Physiology Barbara Heard ...10/26/2014 5 © 2013 Pearson Education, Inc. Figure 16.5b The hypothalamus controls release of hormones from the pituitary gland