Chapter 16
The Endocrine System
J.F. Thompson, Ph.D. & J.R. Schiller, Ph.D. & G.R. Pitts, Ph.D.
Endocrine System: An Overview
The body’s second homeostatic control system
Uses hormones as control agents
Hormones: chemical messengers released into the
blood to regulate specific body functions
Hormones are secreted by endocrine (ductless) glands
and tissues
Endocrinology: the scientific study of hormones and
the endocrine organs
Hormones Regulate:
 Volume & chemical composition of the extracellular fluid (ECF)
 Metabolism and energy balance
 Contraction of smooth and cardiac muscle fibers and many
glandular secretions
 Homeostasis during normal and emergency conditions
 Some immune system activities
 Coordinated, sequential growth, development, and maturation
 Reproduction by regulating:
gamete production
 fertilization
 nourishment of the embryo and fetus
 labor and delivery
 lactation for nourishment of the infant

Nervous vs. Endocrine Systems
 rapid
 action potentials (nerve
impulses) propagated via
nerve fibers
 neurotransmitters released at
specific effector(s)
 nerve impulses are brief
(msecs/seconds), although
control can be sustained
 response of effectors is of
relatively short duration
(seconds/minutes)
 slower
 hormones released into body
fluids; circulated throughout
the body in the blood
 all body cells exposed; only
target cells with receptors
respond
 hormones persist for
seconds/hours/days
 responses of target cells may
last seconds/hours/days,
even weeks/months
Endocrine versus
Exocrine Glands
 All glands
have extensive capillary blood
supply
 form a discrete structure/organ

 Endocrine glands

secrete hormones into
surrounding tissue fluid by
exocytosis and the blood
transports them to target cells
 Exocrine glands

secrete various compounds by
exocytosis into a duct system
 Mixed glands

both endocrine and exocrine
functions
Six Pure Endocrine
Glands
pineal
pituitary
thyroid
parathyroid
adrenal cortex/medulla
thymus
Other Endocrine
System Components
mixed glands:
pancreas
 gonads: ovaries & testes

other endocrine tissue:
stomach and intestines
 skin and adipose tissue
 heart
 kidneys
 placenta

neuroendocrine “organs”:

Hypothalamus/Pituitary gland
Types of Chemical Regulators
Circulating hormones (endocrines): travel via
the blood to reach all tissues, and may affect
distant target cells
Local hormones – diffuse into local interstitial
fluid, reach and affect only local target cells
paracrine
- acts on target cells close to the site
of release
autocrine - acts on the same cell which secreted
it
for the various immune system local hormones,
see Chapter 21 (cytokines, lymphokines, etc.)
Circulating vs. Local Hormones
Local hormone molecules are usually short lived, and
inactivated quickly
Circulating hormone molecules linger in the
bloodstream, and exert their effects for minutes or
hours
 inactivated
by enzymes in the target tissues or in the
bloodstream or in the liver; some hormones are also
eliminated by the kidneys
 kidney
or liver disease – may cause problems due to
increased hormone levels
The Chemistry of Hormones
Two main chemical classes of circulating hormones:

I.
Amino acid based:
amines - from single amino acids
peptides – short sequences of amino acids
proteins - long chains of amino acids
II. Steroids: synthesized from cholesterol

A third category exists, if local hormones are
included:
eicosanoids: synthesized from a cell membrane fatty acid
(arachidonic acid)
Mechanisms of Hormone Action
Hormones may alter cell activities and metabolism by:
 Changing
membrane permeability or membrane
potential by opening or closing gated ion channels
 Synthesis
of proteins, lipids, or carbohydrates or certain
regulatory molecules within the cell
 Enzyme
activation or deactivation
 Induction
or suppression of secretory activities
 Stimulation
of mitosis (and meiosis in the stem cells in
the gonads)
Second Messenger Systems
Most amino acid, peptide and protein
hormones:
 Are
water soluble/lipid insoluble (hydrophilic)
 Cannot
 Need
cross the cell membrane
a second messenger to exert their effects
Second Messenger Systems
Since amino acid based hormones cannot enter cells,
a 2nd messenger must convey the hormone signal to
the inside of the cell (the hormone is the 1st
messenger)
Molecules that serve as second messengers include:
 cyclic
AMP  activates protein kinases
 cyclic GMP  inactivates protein kinases
 IP3 (inositol triphosphate)  Ca2+ ions released
 Ca2+ ions that may bind to calmodulin
Cyclic AMP (cAMP)
1) Hormone A (excitatory) binds
1) Hormone B (inhibitory) binds
membrane receptor, activating Gs
its membrane receptor,
2) Gs stimulates adenylate cyclase (AC)
activating Gi
3) AC forms cAMP from ATP
2) Gi inhibits adenylate cyclase
4) cAMP activates Protein Kinase A
3) Antagonistic control
5) PKA: activates/deactivates other
enzymes; stimulates cell secretion;
opens ion channels, etc.
Second Messengers (cont.)
 Two second messengers may work together (e.g., IP3 & Ca2+)
 Twice as much activation
 Activate enzymes and trigger other intracellular activities
Amplification by Hormones
Hormones are in very low concentrations in body
fluids
They bind reversibly to target cell membrane
receptors
Second messengers initiate a cascade of events (a
“snowball” effect) because they activate enzymes that
act on other enzymes
This cascade effect amplifies the effect of small
quantities of hormone binding to cells
Amplification: the Cascade Effect
For instance, consider a single hormone molecule
binding to a specific receptor on a cell surface
 It
may activate 10 membrane proteins
 Each
membrane protein may activate 10 adenylate
cyclase enzymes to produce 1000 cAMP’s
 This
produces a total of 100,000 second messengers in
the cell which act on various cytoplasmic enzymes
 Each
enzyme may then activate hundreds/thousands of
other protein molecules
Steroid Hormone
Action
 Steroid hormones (derived from
cholesterol) are lipid soluble and
penetrate the cell membrane
 Bind to cytoplasmic receptors inside
the cell
 Hormone-receptor (h-r) complex
enters the nucleus, binds to a DNA
receptor protein
 This causes transcription of certain
genes, and thus produces specific
proteins
 This direct gene activation is a
slower process, but with longer
lasting effects
Target Cell Specificity
Target cells have specific cell surface or
cytoplasmic receptors which bind to a specific
hormone
A target cell has 2,000 to 100,000 receptors for each
hormone to which they respond
 down-regulation:
reduction in the number of
receptors when a hormone is present in excess so
target tissues become less sensitive
 up-regulation:
increase in the number of receptors
when hormone is deficient so that target tissues
become more sensitive
Hormone Interactions at Targets
Permissveness: one hormone allows another hormone
to cause an effect
 ex:
thyroid hormone permits reproductive hormones to
cause their effects on reproductive development
Synergism: effect of two hormones acting together is
greater than either acting alone
 ex:
glucagon and epinephrine together cause more
increase in blood glucose than either alone
Antagonism: one hormone has an opposite effect to
another hormone
 ex:
glucagon elevates blood glucose, insulin lowers
blood glucose
Control of Hormone
Release
1. Humoral Control/Autocontrol:
levels of substances in the blood
regulate the release of the
hormone, e.g.:

Ca2+ levels in blood regulate PTH
release by the parathyroid gland

Glucose levels in blood regulate
insulin and glucagon release by the
pancreatic islets

Na+ and K+ levels in the blood
regulate aldosterone release by the
adrenal cortex
Control of Hormone
Release
2. Nervous System Control: neural
input stimulates the release of
specific hormones, e.g.:

Sympathetic ANS stimulation of the
adrenal glands cause them to release
epinephrine and norepinephrine

Nerve impulses from the
hypothalamus cause oxytocin release
from the posterior pituitary during
labor or breast feeding

Nerve impulses from hypothalamus
cause ADH release from the posterior
pituitary when water concentration of
blood declines
Control of Hormone
Release
3. Hormonal Control: hormones
stimulate the release of other
hormones

Neurohormones from the
hypothalamus stimulate the
anterior pituitary to release
hormones which, in turn,
stimulate the thyroid gland, the
adrenal cortex, and the gonads,
respectively, to release their
hormones
What To Know About Every
Endocrine Organ For The Exam
Name and location of each endocrine gland
Names and acronyms of hormones secreted by each
endocrine gland
Chemical class of the hormone(s) (amine,
peptide/protein, or steroid)
Release mechanisms for the hormone(s)
Antagonistic control to reduce the release of the
hormone(s)
Target tissues or cells for each hormone
Major responses of the target tissues or cells to each
hormone
The Pituitary Gland
 Two structural components with different embryological
origins
Anterior Lobe
Posterior Lobe
(Adenohypophysis)
(Neurohypophysis)
“The Master Gland”
 The pituitary gland has two
functional components

Anterior pituitary




Adenohypophysis
Primarily glandular tissue
Synthesizes protein
hormones
Posterior pituitary




Neurohypophysis
Primarily neuosecretory cells
(their cell bodies in the
hypothalamus)
Secretes peptide
hormones
Some support/glial cells
The Pituitary Gland
 Connected to the
hypothalamus by the
infundibulum
 Vascular linkage
hypothalamus to the
anterior pituitary
 two capillary beds –
the hypophyseal
portal system

 Nervous linkage
hypothalamus to the
posterior pituitary
 hypothalamic neuron
axons

Regulation of Pituitary Hormone Release
 Anterior pituitary
 hypothalamic
releasing
and inhibiting
hormones/factors
transported via blood
in the hypophyseal
portal system
 Posterior pituitary
 neuroendocrine
release
from neurosecretory
cells
 hormones produced in
hypothalamus and
released from axon end
bulbs in the posterior
lobe
Anterior Lobe / Adenohypophysis
Growth Hormone = human growth hormone (hGH)
 Release
stimulated by GHRH from the hypothalamus
 negative feedback regulation by low blood levels of GH
 inhibited by GHIH (somatostatin) from the hypothalamus

 Actions
targets especially liver, muscle, bone, cartilage; also most
tissues
 stimulates growth, mobilizes fats, elevates blood glucose
(insulin antagonist)

Anterior Lobe / Adenohypophysis
 Growth Hormone

pathologies


hyposecretion – pituitary dwarfism (normal trunk/limb proportions)
hypersecretion
• childhood – pituitary gigantism
• adulthood - acromegaly
Anterior Lobe / Adenohypophysis
Thyroid Stimulating Hormone (TSH)
 Release

stimulated by:
• TRH from hypothalamus
• indirectly by pregnancy and body temperature

inhibited by negative feedback from the thyroid hormones
and GHIH (somatostatin)
 Actions
targets thyroid gland
 stimulates thyroid hormone release (T3 and T4)

Anterior Lobe / Adenohypophysis
 Thyroid Stimulating Hormone (TSH)

pathologies


hyposecretion – hypothyroidism
hypersecretion -- hyperthyroidism
myxedema
thyroid cretinsim
exophthalmia
Anterior Lobe / Adenohypophysis
Adrenocorticotropic Hormone (ACTH)
 Release
stimulated by corticotropin releasing hormone (CRH) from
hypothalamus
 inhibited by negative feedback by glucocorticoids from
adrenal gland (and by chronic use of therapeutic antiinflammatory steroids)

 Actions
targets adrenal cortex
 stimulates release of glucocorticoids (and to a lesser
degree -- gonadocorticoids, and mineralocorticoids)

Anterior Lobe / Adenohypophysis
Adrenocorticotropic Hormone
(ACTH)
 pathologies
hyposecretion – Addison’s Disease
 hypersecretion – Cushing’s Disease
(pituitary tumor)

hyperpigmentation
Cushing’s Disease - edema
Anterior Lobe / Adenohypophysis
Follicle Stimulating Hormone (FSH)
 Release
stimulated by gonadotropin releasing hormone (GnRH)
from hypothalamus
 inhibited by negative feedback

• estrogen and inhibin in females
• testosterone and inhibin in males
 Actions

targets ovaries and testes
• female
– stimulates ovarian follicle to mature
– stimulates production of estrogen
• male - stimulates sperm production
Anterior Lobe / Adenohypophysis
Luteinizing Hormone (LH) [Interstitial Cell Stimulating
Hormone (ICSH) in males]
 Release
stimulated by GnRH
 inhibited by negative feedback

• estrogen and progesterone in females (except during LH surge)
• testosterone in males
 Actions
targets ovaries and testes
 stimulates

• females - ovulation and production of estrogen and especially
progesterone
• males – production of androgens, e.g., testosterone
Anterior Lobe / Adenohypophysis
Prolactin
 Release
stimulated by an unidentified Prolactin Releasing
Hormone (PRH) from the hypothalamus
 enhanced by estrogens, birth control pills and breast
feeding
 inhibited by:

• dopamine = Prolactin Inhibiting Hormone (PIH)
• lack of neural stimulation (no suckling)
 Actions
targets breast secretory tissue
 stimulates milk production for lactation

[Note: The seventh anterior pituitary hormone, Melanocyte
Stimulating Hormone = MSH is of limited importance in humans.]
Posterior Lobe / Neurohypophysis
Oxytocin
 Release

positive feedback
• uterine stimulation (stretch) and suckling stimulate the
hypothalamus to release oxytocin from the posterior pituitary
• stimulates uterine contractions (labor) and milk letdown
• increases feedback for more oxytocin release

inhibited by lack of these stimuli
 Actions
targets smooth muscle of the uterus and the breast
 stimulates uterine contractions and milk ejection/letdown

Posterior Lobe / Neurohypophysis
Antidiuretic Hormone (ADH) or Vasopressin
 Release

stimulated by impulses from hypothalamus in response
to:
• increased osmolarity (dehydration)
• decreased blood volume or blood pressure
• stress

inhibited by adequate hydration or ethanol ingestion
 Actions

(1) targets kidney (ADH effect)
• stimulates kidney tubule cells to reabsorb water
• NaCl (salt) will be conserved passively to some degree

(2) targets vascular smooth muscle to constrict
• elevates blood pressure (vasopressin effect)
Thyroid Gland
 Located in the anterior neck
inferior to the larynx
(“Adam’s apple”)
 Two lateral lobes connected
by isthmus
 The largest pure endocrine
gland in the body
 Has a rich blood supply
Thyroid gland (continued)
 Structure
 Spherical follicles
lined with cuboidal
follicular cells
 site of production of
thyroid hormones




thyroxine (T4)
(tetraiodo- thyronine)
triiodothyronine (T3)
amine hormones
 Parafollicular (C cells)
between follicles
 produce calcitonin
(thyrocalcitonin)
 a protein hormone

The interior of the follicle contains the thyroid
“colloid” which is the inactive storage form of
thyroid hormones, called thyroglobulin.
Thyroid Gland (continued)
Thyroid Hormones
 thyroxine
(T4) and triiodothyronine (T3)
 amine
hormones – unusual in penetrating its target
cells to bind with cytoplasmic receptors
 formed
 two
from an amino acid (AA) – tyrosine
linked tyrosines with iodine atoms covalently bound
4 iodine atoms - thyroxine (T4) = tetraiodothyronine
 3 iodine atoms - triiodothyronine (T3)

Thyroid Hormones (continued)
 Actions
targets all tissues except adult brain, spleen, testes, uterus and
thyroid gland
 carried in blood attached to a transport protein, only active when
freed from the transport protein to diffuse into the tissues
 stimulates glucose metabolism




increases basal metabolic rate
increases body heat = thermogenesis
important regulator of growth and development in conjunction
with hGH
 Regulation
decreased levels of thyroid hormones stimulate TRH and TSH
 hypothalamic TRH stimulates the anterior pituitary to release TSH
which stimulates the thyroid to release thyroid hormones

Thyroid Gland Pathologies
 Hypothyroidism*

adults – myxedema



infants – cretinism


*
lethargic, low metabolism,
puffy eyes, easily chilled,
mental impairment
if due to lack of iodine, then
a goiter - increased thyroid
size
short, thick body, mental
retardation
improper development
Note: the defect may be in the
pituitary gland or in the thyroid gland
itself
Thyroid Gland Pathologies
 Hyperthyroidism: Graves
disease among others

body produces
autoantibodies which bind
and stimulate the TSH
receptor inappropriately

stimulates excess thyroid
hormone production

causes elevated metabolic
rate, sweating, rapid
heartbeat, high blood
pressure, nervousness,
bulging eyes (exophthalmia)
* Note: the defect may be in the pituitary
gland or in the thyroid gland itself
Thyroid Hormones (continued)
(Thyro)Calcitonin
A
protein hormone
 Release
from parafollicular (C) cells in thyroid tissue (between the
follicles)
 triggered by elevated blood calcium levels

 Actions
targets bones, primarily in childhood
 inhibits osteoclast activity (stops bone resorption)
 stimulates osteoblasts for calcium uptake and
incorporation into hydroxyapatite in the bone matrix
 Net effect: decreases blood Ca2+ levels

Parathyroid Glands
 Typically four small glands
on the posterior surface of
the thyroid gland
 Filled with chief (principal)
cells which secrete
parathyroid hormone (PTH or
parathormone)
 Oxyphil cells – larger cells,
function unknown
 PTH is a protein hormone
Parathyroid Hormone (PTH)
 Release - negative feedback
stimulated by low blood Ca2+
levels
 inhibited by high blood Ca2+ levels

 Targets:
Bone: osteoclasts dissolve matrix
liberating Ca2+ and PO4- ions
 Intestine: absorb Ca2+ and PO4ions
 Kidney: reabsorb Ca2+ and
eliminate PO4- ions
 activates vitamin D to active
vitamin D3 (calcitriol), enhances
Ca2+ absorption at the intestine
 Net effect: elevates blood Ca2+
levels

The Adrenal Glands
 Paired glands near the
tops of the kidneys
 Two separate parts:

adrenal medulla



interior of the gland
derived from nervous
tissue – works with the
sympathetic division of
the ANS
adrenal cortex


exterior region of gland
made up of three
layers
• zona glomerulosa
• zona fasciculata
• zona reticularis

glandular epithelial
tissue
The Adrenal Cortex
Multi-enzyme pathways convert cholesterol into the
various steroid hormones
Synthetic enzymes are organized in the layers of the
cortex
 zona
glomerulosa (outer)
produces mineralocorticoids (aldosterone)
 controls homeostasis of electrolytes (ions) and water

 zona
fasciculata (middle)
produce glucocorticoids (cortisol)
 involved in glucose metabolism and overall metabolism

 zona
reticularis (inner)
produce male and female gonadocorticoids in small
quantities
 insignificant contribution to reproductive functions

Mineralocorticoids
 Regulate electrolyte (ion) levels, particularly Na+ and K+

movement of other ions (K+, H+, Cl-, HCO3- ,etc.) is linked to Na+
movement

an electrostatic equilibrium must be maintained; therefore if certain
positive ions are returned to the plasma, other positive ions must
move into the urine or negative ions must move to the plasma to
maintain the body fluid electrostatic (charge) equilibrium
water follows Na+ and Cl- by osmosis
 play an important role in blood pressure regulation and regulation
of acid-base balance

 Aldosterone
the primary mineralocorticoid in humans
 causes Na+ and Cl- reabsorption into the blood plasma, by
targeting the kidney, and causes K+ excretion into the urine
 water is conserved passively because it follows NaCl movement

Control of Aldosterone Release
 Aldosterone release from the
zona glomerulosa is regulated
by:
decreasing plasma levels of Na+
and increasing levels of K+
which trigger aldosterone
release
 increasing plasma levels of Na+
and decreasing levels of K+
inhibit aldosterone release
 ACTH



usually does not stimulate
much mineralocorticoid release
but at high levels, ACTH will
stimulate aldosterone
production
The Renin-Angiotensin System
 The kidneys monitor Na+ levels
 If Na+ is low, special kidney
cells release renin (enzyme)
 Renin catalyzes the formation of
angiotensin I from
angiotensinogen
 ACE (angiotensin converting
enzyme) catalyzes formation of
angiotensin II (hormone)
 AII has many functions
 stimulates aldosterone
release from adrenal cortex
 increases Na+ reabsorption at
the kidney
 potent vasoconstrictor
 stimulates thirst
of lungs
Atrial Natriuretic Peptide (ANP)
 Aldosterone is inhibited by Atrial
Natriuretic Peptide (ANP)

ANP is released from the heart’s
atrial walls in response to:



increase in blood pressure
increased stretch of the atrial
walls
ANP actions



increases Na+ excretion and K+
retention at the kidney
inhibits aldosterone release and
the renin-angiotensin system
decreases blood pressure
Glucocorticoids
 Influence cellular metabolism and respond to stress and
inflammation
 Cortisol (hydrocortisone), cortisone, corticosterone
 Release (from the zona fasciculata)
regulated by negative feedback
 stimulated by ACTH from the anterior pituitary
 negative feedback inhibition by increasing levels of glucocorticoids

 Actions
targets most tissues
 promotes hyperglycemia (insulin antagonist)
 mobilizes fats for catabolism (energy production)
 mobilizes protein for catabolism (energy production)
 resistance to stress by providing nutrient building blocks
 depresses inflammatory response and immune system as a
normal part of immune system regulation

Gonadocorticoids
Production by the adrenal cortex is relatively
unimportant
Produced in small amounts at the zona reticularis
Both males and females produce small quantities of
both androgens and estrogens, even before puberty
 androgens

= male sex hormones
primarily androstenedione - a precursor to testosterone
 estrogens
The Adrenal Medulla
A modified sympathetic ganglion in which the
postganglionic neurons have become specialized
neurosecretory cells
Produces two very chemically similar amine hormones
Stimulated by the sympathetic nervous system to
release epiniphrine and norepinephrine (NE) into the
bloodstream, targeting cells with NE receptors
Causes brief excitatory responses
 the
same responses as elicited by the sympathetic
nervous system stimulation
 these circulating hormones bind to the same adrenergic
receptors in target organs that are stimulated by the
ANS
Major Endocrine Glands
 The Adrenal Gland and Stress
short
term
long
term
The Pancreas
 a soft, fragile organ in abdomen beneath
the stomach
 a mixed gland with both exocrine and
endocrine functions
 acinar cells (exocrine)


secrete various digestive enzymes
pancreatic islets [of Langerhans]
(endocrine)




produces protein hormones
alpha cells secrete glucagon
beta cells secrete insulin
other endocrine cell types present in
small numbers
Glucagon from Alpha Cells
 Release – direct assesment of the
blood glucose (humoral influence)
 triggered by hypoglycemia
(decreased blood glucose levels)
 also stimulated by increased
plasma levels of amino acids
 Actions
 primarily targets the liver
 increase release of glucose into
blood (insulin antagonist)


stimulates glycogenolysis
(breakdown of glycogen to
glucose)
stimulates gluconeogenesis
(synthesis of “new”glucose from
amino acids, lipids and lactic acid)
Insulin from Beta Cells
 Release - direct assesment of the
blood glucose (humoral influence)
 triggered
by hyperglycemia
(increased blood glucose
levels)
 triggered by increased levels
of amino acids and fatty acids
 Actions

targets most cells in the body
(except nervous tissue) to increase
glucose uptake




increases glucose metabolism
increases glycogen synthesis
increases conversion of glucose to
fat
inhibits breakdown of glycogen and
gluconeogenesis
Insulin Pathologies - Diabetes
Diabetes mellitus
 insulin
problems result in sustained increased blood
glucose levels
 physiological changes:
polyuria - excessive urination and resulting dehydration
 polydypsia - excessive thirst
 polyphagia - excessive hunger despite hyperglycemia
 often, weight loss over time
 increased susceptibility to injuries and infections
 ketoacidosis - fat metabolism yields ketone bodies
including acetone which can be smelled
 cardiovascular and neurological problems

Types of Diabetes Mellitus
 Type I - insulin-dependent diabetes mellitus (IDDM)
rapid onset of symptoms prior to age 15
 [old name – “juvenile onset”]
 lack of insulin activity - insulin production problems
 beta cells destroyed by the immune system
 daily, frequent dosages of insulin

 Type II - non-insulin-dependent diabetes mellitus (NIDDM)
[old name – “adult onset”]
 usually in overweight individuals
 some insulin is produced by islets but body cells do not respond
adequately to the insulin – a lack of sensitivity
 insulin receptors do not respond to insulin
 management by diet and exercise or by oral antihyperglycemic
drugs

The Gonads
Male – Testes
Female – Ovaries
A Preview of Chapters 27 & 28
The Ovarian Cycle
 Controlled by FSH and LH from the adenohypophysis
 The target organ is the ovary, which becomes responsive at puberty
 The ovary releases estrogens and progesterone in varying proportions
depending on the mix of FSH and LH during the ~28 day cycle
 A midcycle pulse of LH triggers ovulation
ovulation
The Menstrual Cycle
 Is controlled by estrogens and progesterone from the ovary
 The target organ is the uterus, which becomes responsive at
puberty
 The uterine lining increases in anticipation of the arrival of a
developing embryo, if fertilization occurred at the right time
during the ~28 day cycle
 If there is no pregnancy,
the uterine lining will be
sloughed producing a
discharge of tissue and
blood, the “menses”
Pregnancy
 Placental human chorionic
gonadotropin (hCG) provides
the positive feedback loop
between placenta and
ovaries and the anterior
pituitary during pregnancy
 Continued growth of the
placenta in support of the
developing embryo is
controlled by estrogens and
progesterone supplied by
both the ovaries and the
placenta
Endocrine Control of Female Cycles
The Testes
Structure

seminiferous tubules with interstitial cells between the tubules

seminiferous tubules are the site of sperm production

interstitial cells between the tubules secrete male hormones
Brain-Testicular Axis in Males
 Anterior pituitary activity changes
during puberty for males (and
females)


begins to secrete FSH, LH
controlled by GnRH from
hypothalamus
 LH stimulates the interstitial
endocrinocytes


results in testosterone production
negative feedback regulates the
levels
 FSH stimulates sustentacular cells
to produce:


androgen-binding protein (ABP)
inhibin
Testosterone and Other Androgens
Secondary sex characteristics
 muscular
and skeletal growth
heavier, thicker muscle and bones in men than in women
 contributes to epiphyseal closure

 pubic,
axillary, facial and chest hair patterns
oil gland secretion
 laryngeal enlargement deepens the tone of voice

Sexual functions
male sexual behavior and aggression
 spermatogenesis
 sex drive in both male and female

Metabolism - stimulates (“anabolic”) protein synthesis
Other Endocrine Tissues
Heart
 the
atria walls have special endocrine cells that secrete
Atrial Natriuretic Peptide (ANP)
 ANP increases urine output and inhibits Aldosterone
release in response to increased blood volume
GI tract
 enteroendocrine
cells scattered through digestive tract
 several amine and protein hormones which function to
increase or decrease GI secretions and motility
Kidney
 secretes
protein hormone Erythropoietin to target
bone marrow for red blood cell (RBC) production
 secreted in response to low RBC numbers
End Chapter 16