Hormones

It seems like a farfetched notion that a small chemical can enter the bloodstream and
cause an action at a very distant location in the body. Yet this scenario occurs everyday.
The ability to maintain homeostasis and respond to stimuli is largely due to hormones
secreted within your body. Without hormones, you could not grow, maintain a constant
temperature, produce offspring, or perform the basic actions that are essential for life.

The endocrine system produces hormones that are instrumental in maintaining

homeostasis and regulating reproduction and development. A hormone is a chemical
messenger produced by a cell that effects specific change in the cellular activity of other
cells (target cells). Unlike exocrine glands (which produce substances such as saliva,
milk, stomach acid, and digestive enzymes), endocrine glands do not secrete substances
into ducts (tubes). Instead, endocrine glands secrete their hormones directly into the
surrounding extracellular space. The hormones then diffuse into nearby capillaries and
are transported throughout the body in the blood.

The endocrine and nervous systems often work toward the same goal—both influence
other cells with chemicals (hormones and neurotransmitters). However, they attain their
goals differently. Neurotransmitters act immediately (within milliseconds) on adjacent
muscle, gland, or other nervous cells, and their effect is short-lived. In contrast, hormones
take longer to produce their intended effect (seconds to days), may affect any cell, nearby
or distant, and produce effects that last as long as they remain in the blood (up to several
hours).

Hormones can be chemically classified into four groups:

• Amino acid-derived hormones are modified amino acids.

• Polypeptide and protein hormones are chains of amino acids of less than or more
than about 100 amino acids, respectively. Some protein hormones are actually
glycoproteins, containing glucose or other carbohydrate groups.
• Steroid hormones are lipids that are synthesized from cholesterol. Steroids are
characterized by four interlocking carbohydrate rings.
• Eicosanoids are lipids that are synthesized from the fatty acid chains of
phospholipids found in plasma membrane.

Mechanisms of hormone action

Hormones circulating in the blood diffuse into the interstitial fluids surrounding the cell.
Cells with specific receptors for a hormone respond with an action that is appropriate for
the cell. Because of the specificity of hormone and target cell, the effects produced by a
single hormone may vary among different kinds of target cells.

Hormones activate target cells by one of two methods, depending upon the chemical
nature of the hormone:
 • Lipid-soluble hormones (steroid hormones and hormones of the thyroid gland)
diffuse through the cell membranes of target cells. The lipid-soluble hormone then
binds to a receptor protein that, in turn, activates a DNA segment that turns on
specific genes. The proteins produced as result of the transcription of the genes
and subsequent translation of mRNA act as enzymes that regulate specific
physiological cell activity.
• Water-soluble hormones (polypeptide, protein, and most amino acid hormones)
bind to a receptor protein on the plasma membrane of the cell. The receptor
protein, in turn, stimulates the production of one of the following second
messengers:
• Cyclic AMP (cAMP) is produced when the receptor protein activates another
membrane-bound protein called a G protein. The G protein activates adenylate
cyclase, the enzyme that catalyzes the production of cAMP from ATP. Cyclic
AMP then triggers an enzyme that generates specific cellular changes.
• Inositol triphosphate (IP3) is produced from membrane phospholipids. IP3, in
turn, triggers the release of Ca2+ from the endoplasmic reticulum, which then
activates enzymes that generate cellular changes.

Control of hormone production

Endocrine glands release hormones in response to one (or more) of the following stimuli:

• Hormones form other endocrine glands.

• Chemical characteristics of the blood (other than hormones).
• Neural stimulation.

Most hormone production is regulated by a negative feedback system. The nervous

system and certain endocrine tissues monitor various internal conditions of the body. If
action is necessary to maintain homeostasis, hormones are released, either directly by an
endocrine gland or indirectly though the action of the hypothalamus of the brain, which
stimulates other endocrine glands to release hormones. The hormones activate target
cells, which initiate physiological changes that adjust body conditions. When normal
conditions have been restored, the corrective action—the production of hormones—is
discontinued. Thus, in negative feedback, when the original (abnormal) condition has
been repaired, or negated, corrective actions decrease (or are discontinued). For example,
the amount of glucose in the blood regulates the secretion of insulin and glucagons
through negative feedback.

The production of some hormones is regulated by positive feedback. In such a system,

hormones cause a condition to intensify (rather than decrease). As the condition
intensifies, hormone production increases. Such positive feedback is uncommon but does
occur during childbirth (hormone levels build with increasingly intense labor
contractions) and lactation (where hormone levels increase in response to nursing, which
causes milk production to increase).
 The Hypothalamus and Pituitary Glands
The hypothalamus makes up the lower region of the diencephalons and lies just above the
brain stem. The pituitary gland (hypophysis) is attached to the bottom of the
hypothalamus by a slender stalk called the infundibulum. The pituitary gland consists of
two major regions—the anterior pituitary gland (anterior lobe or adenohypophysis) and
the posterior pituitary gland (posterior lobe or neurohypophysis).

The hypothalamus oversees many internal body conditions. It receives nervous stimuli
from receptors throughout the body and monitors chemical and physical characteristics of
the blood, including temperature, blood pressure, and nutrient, hormone, and water
content. When deviations from homeostasis occur or when certain developmental
changes are required, the hypothalamus stimulates cellular activity in various parts of the
body by directing the release of hormones from the anterior and posterior pituitary
glands. The hypothalamus communicates directives to these glands by one of the
following two pathways:

• Communication between the hypothalamus and the anterior pituitary occurs

through chemicals (releasing hormones and inhibiting hormones) that are
produced by the hypothalamus and delivered to the anterior pituitary through
blood vessels. The releasing and inhibiting hormones are produced by specialized
neurons of the hypothalamus called neurosecretory cells. The hormones are
released into a capillary network (primary plexus) and transported through veins
(hypophyseal portal veins) to a second capillary network (secondary plexus) that
supplies the anterior pituitary. The hormones then diffuse from the secondary
plexus into the anterior pituitary, where they initiate the production of specific
hormones by the anterior pituitary. The releasing and inhibiting hormones
secreted by the hypothalamus and the hormones produced in response by the
anterior pituitary are listed in Table 1 . Many of the hormones produced by the
anterior pituitary are tropic hormones (tropins), hormones that stimulate other
endocrine glands to secrete their hormones.
 TABLE 1 Hormone Functions
Hormone (H), Releasing Chemical
Hormone (RH), Or Form*
Source Inhibiting Hormone (IH) Target Action

Hypothalamus
GHRH growth hormone RH PP anterior inhibits release of hGH
pituitary
GHIH growth hormone IH PP anterior stimulates release of
(somatostatin) pituitary hGH
TRH thyrotropin RH PP anterior stimulates release of
pituitary TSH and hGH
GnRH gonadotropin RH PP anterior stimulates release of
pituitary LH and FSH
PRH prolactin RH PP anterior stimulates release of
pituitary PRL
PIH prolactin IH PP anterior inhibits release of PRL
(dopanmine) pituitary
CRH corticotropin RH PP anterior stimulates release of
pituitary ACTH

Anterior pituitary (tropic hormones)

TSH thyroid stimulating H GP thyroid stimulates secretion of
(thyrotropin) T3 and T4
ACTH adrenocortico-tropic PP adrenal stimulates secretion of
hormone cortex glucocorticoids
FSH follicle-stimulating GP ovary, testes regulates oogenesis &
hormone spermatogenesis
LH luteinizing hormone GP ovary, testes regulates oogenesis &
spermatogenesis

Anterior pituitary (hormones)

PRL prolactin PR mammary stimulates production of
glands milk
hGH human growth H PR bone, stimulates growth
(somatotropin) muscle,
various
 Hormone (H), Releasing
Hormone (RH), Or Chemical
Source Inhibiting Hormone (IH) Form* Target Action

Posterior pituitary
OT oxytocin PP uterus, uterine contractions,
mammary release of milk
glands
ADH antidiuretic H PP kidneys, increases water
(vasopressin) sweat glands retention

Thyroid gland
T4 thyroxine AA most body increases rate of
cells cellular metabolism
T3 triiodothyronine AA bone increases rate of
cellular metabolism
calcitonin PP bone decreases blood Ca2+

Parathyroid gland
PTH parathyroid hormone PP bone, increases blood Ca2+
kidneys,
intestine

Adrenal medulla
NE epinephrine (adrenaline) AA blood increases blood sugar,
vessels, constricts blood vessels
liver, heart (fight-or-flight
response)
NE norepinephrine AA blood increases blood sugar
(noradrenaline) vessels, constricts blood vessels
liver, heart (fight or flight
response)

Adrenal cortex
mineralocorticoids (e.g., S kidneys increase reabsorption of
aldosterone) Na+, excretion of K+
glucocorticoids (e.g., S most body increase blood sugar
cortisol) cells
androgens (e.g., DHEA) S general stimulate onset of
puberty, female sex
 Hormone (H), Releasing
Hormone (RH), Or Chemical
Source Inhibiting Hormone (IH) Form* Target Action
drive

Pancreas
glucagon (secreted by PP liver increases blood glucose
alpha cells)
insulin (secreted by beta PP liver, decreases blood glucose
cells) muscle,
adipose
somatostatin (secreted PP alpha & beta inhibits insulin &
by delta cells) cells glucagon release
pancreatic polypeptide PP delta cells inhibits somato-statin &
(from F cells) pancreatic enzymes

Ovaries
estrogen S uterus, menstrual cycle,
general secondary sex
characteristics
progesterone S uterus regulates menstrual
cycle, pregnancy
relaxin PP pelvis, dilates cervix & birth
cervix canal
inhibin PR anterior inhibits FSH release
pituitary

Testes
testosterone S testes, spermatogenesis,
general secondary sex
characteristics
inhibin PR anterior inhibits FSH release
pituitary

Pineal
melatonin AA various regulates biological
clock

Kidney
 Hormone (H), Releasing
Hormone (RH), Or Chemical
Source Inhibiting Hormone (IH) Form* Target Action
erythropoietin GP bone increases blood cell
marrow production
calcitriol (Vitamin d) S intestine increases Ca2+
absorption

Placenta
estrogen S uterus maintains pregnancy,
mammary glands
progesterone S uterus maintains pregnancy,
mammary glands
hCG GP ovary stimulates release of
estrogen &
progesterone
hCS PR mammary prepares mammary
glands glands for lactation

Gastrointestinal tract
gastrin PP stomach stimulates HCI release
GIP gastrin inhibitory PP stomach, inhibits gastric juice
peptide pancreas release, increases
insulin
secretin PP pancreas, stimulates release of
liver enzymes & bile
CCK cholecystokinin PP pancreas, stimulates release of
liver enzymes & bile
serotonin AA stomach stimulates stomach
muscle contraction

Heart
ANP atrial natriuretic peptide PP kidney, decreases blood
adrenal pressure
cortex

Most cells
PG prostaglandins E all cells various
except red
 Hormone (H), Releasing
Hormone (RH), Or Chemical
Source Inhibiting Hormone (IH) Form* Target Action
blood cells
LT leukotrienes E all cells various
except red
blood cells

• Communication between the hypothalamus and the posterior pituitary occurs

through neurosecretory cells that span the short distance between the
hypothalamus and the posterior pituitary. Hormones produced by the cell bodies
of the neurosecretory cells are packaged in vesicles and transported through the
axon and stored in the axon terminals that lie in the posterior pituitary. When the
neurosecretory cells are stimulated, the action potential generated triggers the
release of the stored hormones from the axon terminals to a capillary network
within the posterior pituitary. Two hormones, oxytocin and antidiuretic hormone
(ADH), are produced and released in this way. Their functions are summarized in
Table 1 .

Merck Manual
The endocrine system coordinates functioning between different organs through
hormones, which are released into the bloodstream from specific types of cells within
endocrine (ductless) glands. Once in circulation, hormones affect function of the target
tissue. Some hormones exert an effect on cells of the organ from which they were
released (paracrine effect), some even on the same cell type (autocrine effect). Hormones
can be peptides of various sizes, steroids (derived from cholesterol), or amino acid
derivatives.

Hormones bind selectively to receptors located inside or on the surface of target cells.
Receptors inside cells interact with hormones that regulate gene function (eg,
corticosteroids, vitamin D, thyroid hormone). Receptors on the cell surface bind with
hormones that regulate enzyme activity or affect ion channels (eg, growth hormone,
thyrotropin-releasing hormone).

Hypothalamic-Pituitary Relationships

Peripheral endocrine organ functions are controlled to varying degrees by pituitary

hormones. Some functions (eg, secretion of insulin by the pancreas, primarily controlled
by the plasma glucose level) are controlled to a minimal extent, whereas many (eg,
secretion of thyroid or gonadal hormones) are controlled to a great extent. Secretion of
pituitary hormones is controlled by the hypothalamus.
The interaction between the hypothalamus and pituitary (hypothalamic-pituitary axis) is a
feedback control system. The hypothalamus receives input from virtually all other areas
of the CNS and uses it to provide input to the pituitary. In response, the pituitary releases
various hormones that stimulate certain endocrine glands throughout the body. Changes
in circulating levels of hormones produced by these endocrine glands are detected by the
hypothalamus, which then increases or decreases its stimulation of the pituitary to
maintain homeostasis.

The hypothalamus modulates the activities of the anterior and posterior lobes of the
pituitary in different ways. Neurohormones synthesized in the hypothalamus reach the
anterior pituitary (adenohypophysis) through a specialized portal vascular system and
regulate synthesis and release of the 6 major peptide hormones of the anterior pituitary.
These anterior pituitary hormones regulate peripheral endocrine glands (the thyroid,
adrenals, and gonads) as well as growth and lactation. No direct neural connection exists
between the hypothalamus and the anterior pituitary. In contrast, the posterior pituitary
(neurohypophysis) comprises axons originating from neuronal cell bodies located in the
hypothalamus. These axons serve as storage sites for 2 peptide hormones synthesized in
the hypothalamus; these hormones act in the periphery to regulate water balance, milk
ejection, and uterine contraction.

Virtually all hormones produced by the hypothalamus and the pituitary are released in a
pulsatile fashion; periods of such release are interspersed with periods of inactivity. Some
hormones (eg, adrenocorticotropic hormone [ACTH], growth hormone, prolactin) have
definite circadian rhythms; others (eg, luteinizing hormone and follicle-stimulating
hormone during the menstrual cycle) have month-long rhythms with superimposed
circadian rhythms.

Hypothalamic Controls

Thus far, 7 physiologically important hypothalamic neurohormones have been identified

(see Table 1: Principles of Endocrinology: Hypothalamic Neurohormones). Except for
the biogenic amine dopamine, all are small peptides. Several are produced in the
periphery as well as in the hypothalamus and function in local paracrine systems,
especially in the GI tract. Vasoactive intestinal peptide, which also stimulates the release
of prolactin, is one. Neurohormones may control the release of multiple pituitary
hormones. Regulation of most anterior pituitary hormones depends on stimulatory signals
from the hypothalamus; the exception is prolactin, which is regulated by inhibitory
stimuli. If the pituitary stalk (which connects the pituitary to the hypothalamus) is
severed, prolactin release increases, whereas release of all other anterior pituitary
hormones decreases.

Table 1
Hypothalamic Neurohormones
Neurohormone Hormones Affected Effect
Thyrotropin-releasing hormone TSH Stimulate
 Prolactin Stimulate
Gonadotropin-releasing hormone LH Stimulate*

FSH Stimulate*
Dopamine Prolactin Inhibit

LH Inhibit

FSH Inhibit

TSH Inhibit
Corticotropin-releasing hormone ACTH Stimulate
Growth hormone–releasing hormone GH Stimulate
Prolactin-releasing hormone Prolactin Stimulate
Somatostatin GH Inhibit

TSH Inhibit

Insulin Inhibit
TSH = thyroid-stimulating hormone; LH = luteinizing hormone; FSH = follicle-
stimulating hormone; ACTH = adrenocorticotropic hormone (corticotropin);
GH = growth hormone.
*Under physiologic conditions and when administered exogenously in
intermittent pulses. Continuous infusion inhibits the release of LH and FSH.

Many hypothalamic abnormalities (including tumors and encephalitis and other

inflammatory lesions) can alter the release of hypothalamic neurohormones. Because
neurohormones are synthesized in different centers within the hypothalamus, some
disorders affect only one neuropeptide, whereas others affect several. The result can be
undersecretion or oversecretion of neurohormones. Clinical syndromes that result from
the ensuing pituitary hormone dysfunction (eg, diabetes insipidus, acromegaly, Cushing's
syndrome, hypogonadism, hypopituitarism) are discussed in Pituitary Disorders:
Introduction.

Anterior Pituitary Function

The cells of the anterior lobe (which constitutes 80% of the pituitary by weight)
synthesize and release several hormones necessary for normal growth and development
and also stimulate the activity of several target glands.

Adrenocorticotropic hormone (ACTH):

• ACTH is also known as corticotropin. Corticotropin-releasing hormone (CRH) is

the primary stimulator of ACTH release, but antidiuretic hormone plays a role
during stress. ACTH induces the adrenal cortex to release cortisol and several
 weak androgens, such as dehydroepiandrosterone (DHEA). Circulating cortisol
and other corticosteroids (including exogenous corticosteroids) inhibit the release
of CRH and ACTH. The CRH-ACTH-cortisol axis is a central component of the
response to stress. Without ACTH, the adrenal cortex atrophies and cortisol
release virtually ceases.

Thyroid-stimulating hormone (TSH):

• TSH regulates the structure and function of the thyroid gland and stimulates
synthesis and release of thyroid hormones. TSH synthesis and release are
stimulated by the hypothalamic hormone thyrotropin-releasing hormone (TRH)
and suppressed (by negative feedback) by circulating thyroid hormones.

Luteinizing hormone (LH) and follicle-stimulating hormone (FSH):

• LH and FSH control the production of the sex hormones. Synthesis and release of
LH and FSH are stimulated by gonadotropin-releasing hormone (GnRH) and
suppressed by estrogen and testosterone. In women, LH and FSH stimulate
ovarian follicular development and ovulation. In men, FSH acts on Sertoli cells
and is essential for spermatogenesis; LH acts on Leydig cells of the testis to
stimulate testosterone biosynthesis.

Growth hormone (GH):

• GH stimulates somatic growth and regulates metabolism. Growth hormone–

releasing hormone (GHRH) is the major stimulator and somatostatin is the major
inhibitor of the synthesis and release of GH. GH controls synthesis of insulin-like
growth factor 1 (IGF-1, also called somatomedin-C), which largely controls
growth. Although IGF-1 is produced by many tissues, the liver is the major
source. A variant of IGF-1 occurs in muscle, where it plays a role in enhancing
muscle strength. It is less under control of GH than is the liver variant.
• The metabolic effects of GH are biphasic. GH initially exerts insulin-like effects,
increasing glucose uptake in muscle and fat, stimulating amino acid uptake and
protein synthesis in liver and muscle, and inhibiting lipolysis in adipose tissue.
Several hours later, more profound anti–insulin-like metabolic effects occur.
These include inhibition of glucose uptake and use, causing plasma glucose and
lipolysis to increase, which increases plasma free fatty acids. GH levels increase
during fasting, maintaining plasma glucose levels and mobilizing fat as an
alternative metabolic fuel. Production of GH decreases with aging. Ghrelin, a
hormone produced in the fundus of the stomach, promotes GH release from the
pituitary, increases food intake, and improves memory.

Prolactin:

• Prolactin is produced in cells called lactotrophs that constitute about 30% of the
cells of the anterior pituitary. The pituitary doubles in size during pregnancy,
 largely because of hyperplasia and hypertrophy of lactotrophs. In humans, the
major function of prolactin is stimulating milk production. Also, prolactin release
occurs during sexual activity and stress. Prolactin may be a sensitive indicator of
pituitary dysfunction; prolactin is the hormone most frequently produced in
excess by pituitary tumors, and it may be one of the hormones to become
deficient from infiltrative disease or tumor compression of the pituitary.

Other hormones:

• Several other hormones are produced by the anterior pituitary. These include pro-
opiomelanocortin (POMC, which gives rise to ACTH), α- and β-melanocyte-
stimulating hormone (MSH), β-lipotropin (β-LPH), the enkephalins, and the
endorphins. POMC and MSH can cause hyperpigmentation of the skin and are
only significant clinically in disorders in which ACTH levels are markedly
elevated (eg, Addison's disease, Nelson syndrome). The function of β-LPH is
unknown. Enkephalins and endorphins are endogenous opioids that bind to and
activate opioid receptors throughout the CNS.

Posterior Pituitary Function

The posterior pituitary releases antidiuretic hormone (also called vasopressin or arginine
vasopressin) and oxytocin. Both hormones are released in response to neural impulses
and have half-lives of about 10 min.

Antidiuretic hormone (ADH):

• ADH acts primarily to promote water conservation by the kidney by increasing

the permeability of the distal tubular epithelium to water. At high concentrations,
ADH also causes vasoconstriction. Like aldosterone, ADH plays an important
role in maintaining fluid homeostasis and vascular and cellular hydration. The
main stimulus for ADH release is increased osmotic pressure of water in the body,
which is sensed by osmoreceptors in the hypothalamus. The other major stimulus
is volume depletion, which is sensed by baroreceptors in the left atrium,
pulmonary veins, carotid sinus, and aortic arch, and then transmitted to the CNS
through the vagus and glossopharyngeal nerves. Other stimulants for ADH release
include pain, stress, emesis, hypoxia, exercise, hypoglycemia, cholinergic
agonists, β-blockers, angiotensin, and prostaglandins. Inhibitors of ADH release
include alcohol, α-blockers, and glucocorticoids.
• A lack of ADH produces central diabetes insipidus; an inability of the kidneys to
respond normally to ADH causes nephrogenic diabetes insipidus. Removal of the
pituitary gland usually does not result in permanent diabetes insipidus because
some of the remaining hypothalamic neurons produce small amounts of ADH.
Copeptin is coproduced with ADH in the posterior pituitary. Measuring it may be
useful in distinguishing the cause of hyponatremia.

Oxytocin:
 • Oxytocin has 2 major targets: the myoepithelial cells of the breast, which
surround the alveoli of the mammary gland, and the smooth muscle cells of the
uterus. Suckling stimulates the production of oxytocin, which causes the
myoepithelial cells to contract. This contraction causes milk to move from the
alveoli to large sinuses for ejection (ie, the milk letdown reflex of nursing
mothers). Oxytocin stimulates contraction of uterine smooth muscle cells, and
uterine sensitivity to oxytocin increases throughout pregnancy. However, plasma
levels do not increase sharply during parturition, and the role of oxytocin in the
initiation of labor is unclear. There is no recognized stimulus for oxytocin release
in men, although men have extremely low levels.

Endocrine Organs and Tissues

Although their major function is not the secretion of hormones, some organs contain
specialized cells that produce hormones. These organs include the heart, the
gastrointestinal tract, the placenta, the kidneys, and the skin.

In addition, all cells (except red blood cells) secrete a class of hormones called
eicosanoids. These hormones are paracrines, or local hormones, that primarily affect
neighboring cells. Two groups of eicosanoids, the prostaglandins (PGs) and the
leukotrienes (LTs), have a wide range of varying effects that depend upon the nature of
the target cell. Eicosanoid activity, for example, may impact blood pressure, blood
clotting, immune and inflammatory responses, reproductive processes, and the
contraction of smooth muscles.

Antagonistic Hormones
Maintaining homeostasis often requires conditions to be limited to a narrow range. When
conditions exceed the upper limit of homeostasis, specific action, usually the production
of a hormone is triggered. When conditions return to normal, hormone production is
discontinued. If conditions exceed the lower limit of homeostasis, a different action,
usually the production of a second hormone is triggered. Hormones that act to return
body conditions to within acceptable limits from opposite extremes are called
antagonistic hormones.

The regulation of blood glucose concentration (through negative feedback) illustrates

how the endocrine system maintains homeostasis by the action of antagonistic hormones.
Bundles of cells in the pancreas called the islets of Langerhans contain two kinds of cells,
alpha cells and beta cells. These cells control blood glucose concentration by producing
the antagonistic hormones insulin and glucagon:

• Beta cells secrete insulin. When the concentration of blood glucose rises (after
eating, for example), beta cells secret insulin into the blood. Insulin stimulates the
 liver and most other body cells to absorb glucose. Liver and muscle cells convert
the glucose to glycogen (for short-term storage), and adipose cells convert the
glucose to fat. In response, glucose concentration decreases in the blood, and
insulin secretion discontinues (through negative feedback from declining levels of
glucose).
• Alpha cells secrete glucagon. When the concentration of blood glucose drops
(during exercise, for example), alpha cells secrete glucagon into the blood.
Glucagon stimulates the liver to release glucose. The glucose in the liver
originates from the breakdown of glycogon and the conversion of amino acids and
fatty acids into glucose. When blood glucose levels return to normal, glucagon
secretion discontinues (negative feedback).

Another example of antagonistic hormones occurs in the maintenance of Ca2+

concentration in the blood. Parathyroid hormone (PTH) from the parathyroid glands
increases Ca2+ in the blood by increasing Ca2+ absorption in the intestines and
reabsorption in the kidneys and stimulating Ca2+ release from bones. Calcitonin (CT)
produces the opposite effect by inhibiting the breakdown of bone matrix and decreasing
the release of calcium into the blood.