Nervous system vs, Endocrine system
Nervous system
regulates the activities of muscles and glands via electrical impulses
transported through neurons.
Neural control is fast;
its effects are short-lived
Endocrine System
regulates the body’s metabolic activity via hormones that are transported in
the blood.
Hormonal control is slow; its effects are
prolonged
Endocrine vs. Exocrine glands
Endocrine glands secrete
products directly into blood and lymph (body fluids).
o Ductless
o Ex., thyroid gland
Exocrine glands secrete products into ducts that
lead to the surface of a membrane.
o Have ducts
o Ex., sweat glands and salivary glands
Important Hormone Functions
- Reproduction
- Growth and development
- Immune system response
- Maintenance of electrolyte, water, and nutrient balance
of the blood - Regulation of cellular metabolism and energy balance
Major
Endocrine Organs
- Pineal gland
- Hypothalamus
- Pituitary gland
- Thyroid gland
- Parathyroid gland
- Thymus gland
- Adrenal glands
- Pancreas
- Gonads (i.e., ovaries and testes)
Hormone – A chemical substance secreted by one cell that
affects the functions of another cell.
Three
Classes of Hormones
- Amino
acid-based hormones
o Most hormones are this type
o Tend to stay in the blood
- Steroid
hormones
o Synthesized from cholesterol
o Lipid-soluble; able to pass through the
phospholipid membrane
o Include the gonadal hormones and the adrenal
cortical hormones (secreted by the adrenal cortex)
- Eicosanoids (Minor class of hormones)
o Includes the leukotrienes and prostaglandins
Effects of Hormone Action
Hormonal stimulus
usually produces one or more of the following changes:
- Altering plasma membrane permeability or membrane
potential (or both) by opening or closing ion channels. - Stimulates the synthesis of proteins or regulatory
molecules, such as enzymes with in the cell. - Enzyme activation or deactivation (changes metabolism)
- Induction of secretory activity
- Stimulation of mitosis or meiosis.
Two Main Mechanisms of Hormone Action
- Second-messenger
systems – Since proteins/peptides
hormones cannot cross the cell membrane, they must rely on activating
their receptor on the target cell. - Once bound to the receptor, this will cause the
production of a second messenger. - Second messenger – a chemical that is either produced
or released as the result of a hormone binding to the receptor on the
cell membrane. It affects the activities of the intracellular
enzymes. - Due to the presence of second messengers, large
intracellular changes are caused by small amounts of hormone. - Ex., Cyclic AMP (c AMP) mechanism
- The hormone binds to the
receptor and activates a G-protien. - Activation of the G-protein
activates adenylcyclase (the enzyme that produces c AMP) - Adenylcyclase takes AMP and
changes it to its cyclic form, c AMP. - c AMP activates intracellular
protein kinases. - The activated protein kinases
phosphorylate other enzymes. - Phosphorylation of these
enzymes causes cellular changes. - Ex., PIP-Calcium Signal Mechanism
- Similar to the c AMP
mechanism, but calcium ions are the second messenger. - Direct
gene activation – Since steroid hormones are
lipid soluble, they can pass through the phospholipid membrane with
relative ease and travel to the nucleus to activate the desired genes. - Enables the hormone to activate production of
intracellular proteins without the use of a “middle man.” - Directly activates genes so that specific proteins
(such as enzymes) are produced. - REMEMBER: Each gene codes for
a protein. - Steroids bind to a receptor inside the nucleus, thereby
initiating transcription and translation and the production of proteins. - The proteins produced alter intracellular activity.
Factors
Affecting Hormone-receptor Interaction
- Blood levels of the hormone
- Relative numbers of the receptors for that hormone on
or in target cells - Affinity (strength) of the bond between the hormone and
the receptor.
Receptor Dynamism
- Up-regulation – Target cells increase the number of
hormone receptors in response to elevate hormone levels in the blood. - Down-regulation – Target cells decrease the number of
hormone receptors in response to prolonged exposure to high hormone
concentrations in the blood. - Prevents the target cells from overreacting to
persistently high hormone levels
Half-life, Onset, and Duration of Hormone Activity
- Blood concentrations of hormones are dependent upon:
- Rate of release
- Rate of degradation and removal from the body
- Half-life refers to the amount of time in which half of
the amount of hormone becomes inactive or disappears from the blood. - Variation in chemical structure determines the onset of
hormone activity. - Most hormones cause an immediate response (amino-acid
based) - Steroid hormones may take hours to days to have an
affect. - Duration of a hormone – the length of time that a
hormone causes an effect - Is limited, but relatively longer than the short-lived
effects of the nervous system
Interaction of Hormones at Target Cells
- Permissiveness – One hormone cannot exert its full
effects without another hormone being present. - Ex., reproductive hormones and thyroid hormone
- Synergism – More than one hormone produces the same
effects at the target cell and their combined effects are amplified. - Ex., glucagon and epinephrine cause the liver to
release glucose into the blood\ - Antagonism – One hormone opposes the action of another
hormone. - Ex., Insulin lowers blood glucose levels; glucagon
increases blood glucose levels
Negative Feedback System and Hormones
- Most hormones are regulated by a negative feedback
system. - Hormone secretion is triggered by some internal or
external stimulus. As hormone levels rise, they cause the target
organ effects and inhibit further hormone release. - Prevents wide swings in hormone levels
- Concentrations of the hormones in body fluids must be
closely regulated to prevent dysfunction.
Major Types of Stimuli
- Humoral – Stimulation in response to changes in
blood-ion or blood nutrient concentrations
o Ex., Calcium ion levels
or blood glucose levels
- Neural – Stimulation by nerve fibers
·
Ex. Sympathetic nervous
system stimulation of epinephrine release by the
adrenal medulla.
- Hormonal – Stimulation in response to hormones secreted
by other endocrine organs.
o Ex., most hormones
secreted by the anterior pituitary
Nervous System Modulation
- Humoral, neural, and hormonal stimuli and negative
feedback controls can be modified by the nervous system. The final
decisions are made by the nervous system. - Nervous system modulation allows the CNS to override
the endocrine system. It also makes it possible for mental states
and moods to upset normal hormonal balance.
MAJOR ENDOCRINE ORGANS
Pituitary Gland (aka, hypophysis)
- Bi-lobed: anterior pituitary and posterior pituitary
- Infundibulum connects it to the hypothalamus of the
brain which controls pituitary activity - Secretes at least eight (8) major hormones: Growth
hormone (GH), Thyroid-stimulating hormone (TSH), Adrenocorticotropic
hormone (ACTH), Follicle-stimulating hormone (FSH), Leutinizing hormone
(LH), Prolactin (PRL), Antidiuretic hormone (ADH), and oxytocin
o All amino-acid based and utilize
second-messenger mechanisms
- Anterior Pituitary (aka, adenohypophysis)
o Composed of glandular epithelial tissue
o Hypophyseal portal system serves as the only
connection to the hypothalamus and the rest of the body; no neural connection
exists
§ Hypophyseal releasing and inhibiting hormones
are secreted by neurons
in the ventral
hypothalamus and circulate to the anterior pituitary.
o Very little hormone is stored in the secretory
cells of the anterior lobe.
o Manufactures and releases six (6) hormones:
§ Four (4) tropic hormones:
· Thyroid-stimulating hormone (TSH) – stimulates normal development and secretory activity of thyroid
gland
o thyrotropin
o Thyrotropin-relasing hormone (TRH) is produced
by the hypothalamus
§ Induces TSH secretion
o Negative feedback controls TSH and TRH
secretion; thyroid hormone production suppresses the TSH and TRH release; GHIH
is released by the hypothalamus to reinforce inhibition
· Adrenocorticotropic hormone (ACTH) – stimulates the adrenal cortex to release corticosteroid hormones
o corticotropin
o Corticotropin-releasing hormone (CRH) is
produced by the hypothalamus
§ Induces ACTH secretion
§ Has daily rhythm; highest in morning after
wakening
o Rising levels of corticosteroid hormones feed
back and inhibit CRH and ACTH release.
o Factors altering normal ACTH rhythm
§ Fever, hypoglycemia, and all stressors
· Gonadotropins (FSH and LH) – regulate the
function of the gonads
o Gonadotropin-releasing hormone (GRH) is produced
by the hypothalamus
§ Induces secretion of FSH and LH
o Follicle-stimulating hormone (FSH)
§ In both sexes,
· Stimulates gamete (sperm and egg) production and
maturation
§ In females,
· Stimulates estrogen secretion
o Responsible for the growth and development of
egg-containing follicles in the ovaries
· Causes the egg to grow; matures the egg
§ In males,
· Causes the maturation of the sperm
o Leutinizing hormone (LH)
§ In both sexes,
· Promotes the production of gonadal hormones (sex
hormones)
§ In females,
· Acts with FSH to cause the maturation of an
egg-containing ovarian follicle.
· By itself, it triggers ovulation and promotes
synthesis and release of ovarian hormones (estrogen and progesterone).
§ In males,
· Stimulates the interstitial cells of the testes
to produce testosterone.
· aka, interstitial cell-stimulating hormone
(ICSH) in males
§ Gonadal hormones feed back to suppress FSH and
LH release.
§ Prolactin (PRL)
· PRL production is controlled by hypothalamus:
o Prolactin-releasing hormone (PRH) – causes synthesis
and release
o Prolactin-inhibiting hormone (PIH) – suppresses
release
· In females,
o Promotes breast development and stimulates milk
production
o Prolactin levels rise and fall with estrogen
blood levels
o High levels of estrogen – PRH & PRL release
o Low levels of estrogen – PIH release
o Rise in PRL just before menses causes breast
swelling and tenderness in some women.
o In pregnant women, sustained PRH release is
stimulated by infant suckling.
· In males,
o Enhances testosterone secretion in males
· HORMONAL DYSFUNCTION:
o Hypersecretion = hyperprolactinemia
§ Inappropriate lactation, lack of menses,
infertility in females; breast enlargement (gynecomastia) and impotence in
males
§ Growth Hormone (GH) – stimulates body cells to increase in size,
esp. muscle and bone cells; accelerates the rate of mitosis (increases cell
division)
· Important in the growth and development of
children
o Stimulation of the epiphyseal plate = long bone
growth
o Stimulation of skeletal muscle = increase in
muscle mass
· GH concentrations decrease with age
· Direct actions of GH
o Stimulation of liver, skeletal muscle, bone, and
cartilage cells to produce and release IGFs
§ Indirect growth promoting effects of GH via
insulin-like growth factors (IGFs)
· aka, somatomedins
· Growth-promoting proteins produced by the liver,
skeletal muscle, bone and other tissues.
· Action:
o Stimulate uptake of amino acids from the blood
and their incorporation into cellular proteins throughout the body
o Stimulate uptake of sulfur (needed for
chondrotin sulfate) into cartilage matrix
§ In the liver, increase glycogen breakdown and
release of glucose to the blood à Diabetogenic effect
(elevation of blood sugar levels because of GH glucose sparing)
o Anti-insulin action
§ Stimulation of lipolysis; fat release from
adipose cells
§ Increase blood sugar levels
§ Other effects that antagonize insulin
· Regulation of GH by hypothalamus
o Growth hormone-releasing hormone (GHRH) –
stimulates GH release
o Growth hormone-inhibiting hormone (GHIH) – inhibits
GH release
§ Probably triggered by the feedback of GH and
IGFs
§ Also inhibits other adenohypophyseal hormones,
pancreatic and gastrointestinal secretions
· Other regulatory factors affecting GH release
o Rising levels of GH inhibit its own release
o GH secretion has a daily cycle; highest during
evening sleep
· HORMONAL
DYSFUNCTIONS:
o Hypersecretion
§ In children = gigantism
· Abnormally, but proportionally tall
· Epiphyseal plates are still active
§ In adults = acromegaly
· Overgrowth of bones in the face, feet, and hands
· Epiphyseal plates closed
o Hyposecretion
§ In children = pituitary dwarfism
· Abnormally, but proportionally short
· Can be treated to some degree, with early
detection
§ In adults, not usually a problem
· In rare instances, progeria = rapid aging
- Posterior Pituitary (
neurohypophysis)
o Composed of neural tissue
o DOES NOT MANUFACTURE ANY HORMONES; releases two (2) hormones
produced in the hypothalamus: Antidiuretic hormone (ADH) and oxytocin
§ Both hormones are amino acid-based and use the
PIP-calcium second-messenger system
§ When hypothalamic neurons fire, they release the
stored hormones into a capillary bed in the posterior lobe for distribution
throughout the body.
o Maintains its connection with the hypothalamus via the
hypothalamic-hypophyseal tract
§ Arises from the parventricular and supraoptic
nuclei of the hypothalamus
· Paraventricular nuclei produce ADH
· Supraoptic nuclei produce oxytocin
o Oxytocin – stimulates contraction
of smooth muscles in the uterus during labor and causes “let down” and release
of breast milk
§ An example of positive-feed back systems
(stimulation of uterine contractions and milk “let down”)
§ Release triggered by the stretching of the
uterus and cervix
§ Natural and synthetic oxytocic drugs used to
induce labor or hasten normal labor that is progressing too slowly.
· Sometimes used in stop postpartum bleeding and
to stimulate the milk ejection refelex
§ Studies reveal that oxytocin in males and
nonpregnant females is important in sexual arousal and orgasm; “cuddle
hormone,” in non-sexual relationships
o Antidiuretic hormone – prevents wide swings in water balance by helping the body avoid
dehydration and water overload
§ aka, vasopressin
§ Osmoreceptors monitor solute concentration of
the blood
· High concentrations of solutes – synthesis and
release of ADH
o Secretion of ADH
§ Causes the kidney tubule cells to reabsorb more
water from the forming urine and return it to the bloodstream
· Less urine produced; increase blood volume
· As solute concentrations become more dilute,
supraoptic neurons stop depolarizing and ADH release is inhibited.
§ Other triggers of ADH release
· Pain, low blood pressure, nicotine, morphine,
and barbiturates
§ High concentrations of ADH in the blood
· Triggers vasoconstriction = increase in blood
pressure
· Can be caused severe blood loss
§ Effects of alcohol on ADH release
· Alcohol inhibits ADH secretion
· Causes dehydration and hangover associated with
alcohol consumption
§ Other inhibitors of ADH secretion
· Drinking excessive amounts of water
· Diuretic drugs that cause water to be flushed
from the body
o Used to manage some cases of hypertension and
edema typical of congestive heart failure
§ HORMONAL
DYSFUNCTIONS:
· Hypersecretion
o Can be seen:
§ In children with meningitis
§ Following neurosurgery
§ Following hypothalamic injury
§ Ectopic ADH secretion by cancer cells (esp.
pulmonary cancers)
§ Following general anesthesia or administration
of certain drugs
· Syndrome of inappropriate ADH secretion (SIADH)
o Fluid retention
o Headache
o Disorientation due to brain edema
o Weight gain
o Hypo-osmolarity of the blood
· Hyposecretion = diabetes insipidus
o Insufficient amounts of ADH
o Output of copious amounts of urine and intense
thirst
o Can be caused by physical damage to the
hypothalamus or posterior pituitary
Thyroid Gland
· Located in the neck, inferior to the larynx
· The largest pure endocrine gland in the body
· Has two lobes that are subdivided into follicles
o Follicle walls are formed by cuboidal or
squamous epithelial cells called follicle cells
§ Follicle cells produce thyroglobulin
o The central cavity of the follicle stores
colloid
§ Colloid = an amber, viscous glycoprotein
consisting of thyroglobulin attached to iodine atoms
o Parafollicular cells (C cells)
§ Not apart of the follicle; produce calcitonin
· Thyroid hormone is derived from the iodinated
thyroglobulin
o Thyroid hormone (TH)
§ Thyroxine (T4) and triiodothyronine
(T3)
· T4 = the major hormone secreted by thyroid follicles
· T3 = formed at target tissues
§ Targets all tissues of the body except the adult
brain, spleen, testes, uterus, and the thyroid gland itself
§ Stimulates enzymes involved glucose oxidation
· Increase the basal metabolic rate and body heat
production à calorigenic effect
§ Enhances protein synthesis and lipid breakdown
§ Maintains blood pressure
§ Regulator of tissue growth and development
§ Critical for normal skeletal and nervous system
growth and development and reproductive capabilities
o Falling levels of T4 in the blood trigger TSH release
§ Pregnancy, prolonged cold also trigger TSH
release
o Rising levels of T4 feed back and inhibit TSH release
§ Somatostatin (GHIH), rising glucocorticoids and
sex hormones, and excessively high iodine concentrations also inhibit TSH
release
o HORMONAL
DYSFUNCTIONS:
§ Hypersecretion = Grave’s disease
· Elevated metabolic rate, sweating, rapid,
irregular heartbeat, nervousness, weight loss despite adequate food intake, and
exopthalmos (protrusion of the eyeballs).
· Corrected by removal of thyroid gland or
ingestion of radioactive iodine to destroy the most active thyroid cells.
§ Hyposecretion
· In infants = cretinism
o Mental retardation
o Short, disproportionately sized body
o Thick tongue and neck
o Due to a genetic deficiency of the fetal thyroid
gland or a maternal deficiency of dietary iodine
o Reversible, with early detection
o Developmental abnormalities are irreversible
· In adults = myxedema
o Low metabolic rate
o Chills and constipation
o Thick, dry skin and puffy eyes
o Edema
o Lethargy and mental sluggishness (not
retardation)
o Results from lack of iodine
o Enlargement and protrusion of thyroid gland =
endemic goiter
§ Colloid production normal; can’t iodinate it or
make functional TH
· Calcitonin – lowers blood Ca2+ concentration levels
o Produced by the parafollicular cells (or C
cells)
o Direct antagonist of parathyroid hormone
o Targets the skeleton
§ Inhibits osteoclast activity, bone resorption
and release of calcium ions from the bone matrix
§ Stimulates calcium ion uptake and incorporation
into bone matrix
§ Especially important in growing children; less
important in adults
o Control of calcitonin release
§ Regulation short-lived, but rapid
§ Excessive blood levels of Ca2+
(20% above normal) = release of calcitonin
§ Low Ca2+ blood levels inhibit calcitonin secretion
Parathyroid Glands
- Located on the posterior surface of the thyroid glands
- Usually four (4) glands, can be up to eight (8);
sometimes found in other regions of the neck and thorax - Parathyroid hormone (PTH)
– raise blood calcium levels
o Produced by chief cells
o Action:
§ Stimulates osteoclasts to resorb the bone matrix
§ Causes the kidneys to conserve calcium and
excrete phosphate
· Guarantees that the calcium that’s in the blood
stay in the blood, and isn’t used to form bone with phosphate
§ Stimulates conversion of vitamin D in active
form, which causes an increase in calcium absorption by the intestines
o Control of PTH release
§ Falling blood Ca2+ levels = trigger release
§ Hypercalcemia = inhibits release
o Calcium levels in the blood stream are maintained for
§ Muscle contraction
§ Nerve impulse transmission
§ Blood clotting
§ Enzyme activity (acting as cofactors)
o HORMONAL DYSFUNCTIONS:
§ Hypersecretion
· Rare; usually results from parathyroid gland
tumor
· Calcium leached from bones; bones soften and
deform
· Mineral salts are replaced by fibrous connective
tissue
· Ex., osteitis cystica fibrosa = fragile bones,
fracture spontaneously
· Depressed nervous system à weakness of skeletal muscles and abnormal
reflexes
· Formation of kidney stones due to excess salts
precipitating in the kidney tubules
· Deposition of calcium deposits in soft tissues
of the body à metastatic calcification
§ Hyposecretion
· Results from parathyroid gland trauma or removal
during thyroid surgery
· Can also be caused by an extended deficiency of
dietary magenesium (function parathyroidism)
· Excitability of neurons and tetany
· Loss of sensation, muscle twitches, and
convulsions
· Can progress to respiratory paralysis and death
Adrenal (Suprarenal) Glands
- Located on top of the kidneys in humans
- Divided into two major portions
- Adrenal cortex – outer portion of the adrenal gland
- Mainly glandular epithelium
- Site of corticosteroid
synthesis - Steroid hormones are not
stored in cells; rate of release is proportional to their rate of
synthesis - Arranged into three layers
*Zona glomerulosa – mainly produces the mineralcorticoids
The outermost layer of
the cortex
Layer arranged in
spherical clusters of cells
Mineralcorticoids aid in
maintaining water-mineral balance in the blood
Regulate electrolyte
(mineral salt) concentrations in extracellular fluids, esp. Na+ and K+
Aldosterone
Most potent and most
abundant mineralcorticoid
Primary function is to
maintain sodium ion balance (and consequently, blood pressure)
Stimulates transcription
of the Na+, K+ -ATPase, the sodium pump that exchanges K+ for Na+.
Na+ is the most abundant
cation in extracellular fluid.
Excessive sodium intake
and retention may produce hypertension in prone individuals
Reduces excretion of Na+
from the body
Stimulates Na+
reabsorption from the forming urine and its return to the bloodstream;
primarily targets the distal parts of the kidney tubules
Enhances Na+
reabsorption from perspiration, saliva, and gastric juice
Aldosterone secretion:
Induced by high K+
levels; low Na+ levels; decreasing blood pressure and volume
Inhibited by low K+
levels; high Na+ levels; increasing blood pressure and volume
Regulation of secretion
Plasma electrolyte
concentrations directly cause release
Renin-angiotensin system:
A. Kidneys
release renin when blood electrolytes or blood pressure gets too low.
B. Renin is an enzyme. It starts the conversion of
angiotensin into angiotensin II
C. Angiotensin II stimulates aldosterone
secretion (among other things).
· ACTH –Severe stress can cause a rapid rise in
ACTH and seems to induce aldosterone release and all of the other effects
listed above.
· Atrial natriuretic peptide – inhibits rennin and
aldosterone secretion - produced when blood pressure gets too high.
Zona fasciculata – mainly produces the glucocorticoids
The middle layer of the
cortex
Layer arranged in linear
cords
Glucocorticoids control metabolism rates in most cells; helps provide resistance
to various stressors (Ex., diseases, injury, toxicants)
Cortisol - major
gluccocorticoid – keeps blood glucose levels constant
Inhibits the synthesis
of proteins
Promotes the release of
fatty acids (used to make energy)
Stimulates
gluconeogenesis (the production of new glucose from non-carbohydrate sources)
Regulated by negative
feedback
HORMONAL DYSFUNCTIONS:
Hypersecretion =
Cushing’s disease
Hyperglycemia, loss of
muscle and bone protein; increased water in the blood and tissues à hypertension and edema
Hyposecretion =
Addison’s disease = caused by insufficient production of glucocorticoids and
mineralcorticoids
Weight loss,
hypertension, dehydration, low glucose and sodium levels in the blood, bronze
skin
Zona reticularis – mainly produce small amounts of gonadocorticoids
Innermost layer of the
cortex
Netlike arrangement
Gonadocorticoids are sex
hormones
Adrenal medulla
Interior portion of the
gland
Part of the sympathetic
division of the ANS
Innervated directly by
the CNS
Secrete catecholamines (epinephrine and
norepinephrine)
Instrumental in
fight-or-flight response
Increase in blood
glucose levels; constriction of blood vessels; faster heartbeat (raises the
blood pressure); diversion of blood from non-essential organs to the brain,
heart, and skeletal muscles
Short-lived response
The Pancreas
- Located posterior to the stomach; attached to the small
intestine - Both exocrine (via acinar cells) and endocrine (alpha
and beta cells) functions - Islet of Langerhans
Alpha cells – secrete glucagon
Increases blood sugar
levels when they get low
Stimulates
gluconeogenesis in the liver
Promotes breakdown of
glycogen
Causes glucose
release by the liver
Inhibited by
somatostatin
Beta cells – secrete insulin
Decreases blood glucose
levels when they get high
Promotes the movement of
glucose through the cell membranes
Stimulates the storage
of both glucose and fats
Stimulates glycogen and
protein synthesis
HORMONAL DYSFUNCTIONS:
Type I –Juvenille onset diabetes = insufficient insulin production
Type II – Adult onset diabetes = insulin does not affect the cells of the body
Reproductive Glands
- Ovaries
- Secrete estrogen and progesterone
- Actions
- Regulate menstruation
- Regulate maturation of the
female sex organs - Involved in helping to
produce female secondary sexual characteristics - Testes
- Secrete testosterone
- Regulates maturation of the
male sexual organs - Produces males secondary
characteristics
Pineal Gland
- Attached to the thalamus
- Innervation comes from postganglionic sympathetic
fibers - Secretes melatonin
- May help control circadian rhythms
- Inhibits gonadotropin secretion (FSH, LH) in children;
regulates the onset of puberty and allows children to sleep more - Melatonin secretions higher at night; light seems to
inhibit production
Thymus
- Located between the lungs
- Size diminishes with age
- Produces thymosin – Hormone responsible for the
maturation of T-lymphocytes - Necessary for proper immune system function
Other
Hormone-producing Structures
- Kidneys – erythropoietin (RBC production)
- Heart – Atrial natriuretic protein (response to high
blood pressure) - Placenta – pregnancy hormones
- GI tract mucosa
- Skin – Cholecalciferol = inactive vitamin D