This file is comprised of several hormones of human body along with their sources and mechanisms of action. Each and every gland and their secreting hormones have been covered under this 7 paged file

1. HORMONES(PHYSIOLOGY & PHARMACOLOGY)
PHYSIOLOGY OF HORMONES -
Source of hormones Hormones Mechanisms of action
Hypothalamus 1. Thyrotropin Releasing
Hormone(TRH)
2. Corticotropin
Releasing
Hormone(CRH)
3. Growth Horomone
Releasing
Hormone(GHRH)
4. Growth Hormone
Inhibitory
Hormone(GHIH)[Som
atostatin]
5. Gonadotropin
Releasing
hormone(GnRH)
1. Following secretion at the median eminence, TRH
travels to the anterior pituitary via the hypophyseal
portal system where it binds to the TRH receptor
stimulating the release of thyroid-stimulating hormone
from thyrotropes through the feed-back control
mechanism and prolactin from lactotropes.
2. CRH acts via 2 distinct G protein-coupled receptors,
namely, CRHR1 and CRHR2. In the anterior
pituitary, CRHR1 mediates the release of ACTH in
response to CRH.
3. GHRH, produced by hypothalamic neurons found
predominantly in the arcuate nucleus, stimulatesGH
secretion by binding to a specific GPCR on
somatotropes.
Upon binding GHRH, the GHRH receptor couples to
Gs to raise intracellular levels of cyclic AMP and
Ca²+, thereby stimulating GHsynthesis and secretion.
4. Somatostatin binds to 5 subtypes of somatostatin
receptors (SSTRs), which are all Gi-protein-coupled
transmembrane receptors that inhibits adenylyl cyclase
upon activation. By inhibiting intracellular cyclic AMP
and Ca2+ and by a receptor-linked distal effect on
exocytosis, SSTRs block cell secretion. SSTR1
mediates an antisecretory effect on growth hormone,
prolactin and calcitonin.
5. It acts via G-protein coupled receptors on
gonadotropes to stimulate synthesis and secretion of
the gonadotropin hormones luteinizing hormone and
follicle-stimulating hormone. These receptors couple
primarily via G-proteins of the Gq/ll family, driving
activation of phospholipases C and mediating GnRH
effects on gonadotropin synthesis and secretion.

2. Source of hormones Hormones Mechanisms of action
Anterior Pituitary 1. Growth hormone(GH)
2. Prolactin(PRL)
3. Adrenocorticotrophic hormone
(ACTH,corticotrophin)
4. Melanocyte Stimulating
Hormone(MSH)
5. Gonadotropic
Hormones(follicle stimulating
hormone & luteinizing
hormone)[FSH & LH]
1. growth hormone (hGH) stimulates skeletal growth,
which is accomplished at the epiphyseal plates at
the ends of a growing bone. Growth and
metabolism of epiphyseal plate cells are directly
stimulated by GH and one of its mediators, IGF-I
(insulin-like growth factor).hGH binds to the
human growth hormone receptor (GHR). Upon
binding, hGH causes dimerization of GHR, activation
of the GHR-associated JAK2 tyrosine kinase, and
tyrosyl phosphorylation of both JAK2 and GHR.
These events recruit and/or activate a variety of
signaling molecules, including MAP kinases, insulin
receptor substrates, phosphatidylinositol 3' phosphate
kinase, diacylglycerol, protein kinase C, intracellular
calcium, and Stat transcription factors. These
signaling molecules contribute to the GH-induced
changes in enzymatic activity, transport function, and
gene expression that ultimately culminate in changes
in growth and metabolism.
2. A specific prolactin receptor is expressed on the
surface oftarget cells, which is structurally and
functionally analogousto GH receptor: action is
exerted by transmembrane activationof JAK—
cytoplasmic tyrosine protein kinases and STAT.
3. Acting through MC2 receptors, tetracosactide.
Through alteration of intracellular cAMP concentration
 alteration of protein kinase A regulation of cell
function: Ca2+ acting as third messengerin some
situations. ACTH action is mediated not only by
cyclic adenosine monophosphate (cAMP), but also
by calcium (Ca2+), both interacting closely through
positive feedback loops to enhance steroid secretion.
4. Melanocyte stimulating hormone acts on melanocortin
receptors, of which five (MC1–5) have been
cloned. These are G protein-coupled receptors
(GPCRs) that activate cAMP synthesis. Melanin
formation is controlled by the MC1 receptor. MC1
and MC3 receptors mediate the immunomodulatory
effect of MSH.
5. Distinct LH and FSH receptors are expressed onthe
target cells. Both are G protein coupled receptors
whichon activation increase cAMP production. This in
turnstimulates gametogenesis and conversion of
cholesterol topregnenolone—the first step in

3. 6. Thyroid Stimulating
Hormone(TSH)
progesterone, testosterone andestrogen synthesis. n
the testes FSH receptor is expressedon seminiferous
(Sertoli) cells while LH receptor is expressedon
interstitial (Leydig) cells. In the ovaries FSH
receptorsare present only on granulosa cells, while
LH receptors arewidely distributed on interstitial cells,
theca cells, preovulatorygranulosa cells and luteal
cells.
6. The TSH receptor present on thyroid cells is a
GPCR whichutilizes the adenylyl cyclase-cAMP
transducer mechanism(by coupling to Gs protein) to
produce its effects. In humanthyroid cells high
concentration of TSH also inducesPIP2 hydrolysis by
the linking of TSH receptor to Gq protein.The
resulting increase in cytosolic Ca2+ and protein
kinase Cactivation may also mediate TSH action,
particularlygeneration of H2O2 needed for oxidation
of iodide andiodination of tyrosil residues.
Posterior pituitary
Gland
1. Vasopressin or Anti Diuretic
Hormone(ADH)
2. Oxytocin
1. There are three classes of receptor: V1A, V1B
and V2. All are GPCRs. V2 receptors stimulate
adenylyl cyclase, which mediates the main
physiological actions of vasopressin in the
kidney, where as the V1A and V1B receptors
are coupled to the phospholipase C/inositol
trisphosphate system. The receptor for
oxytocin(OTreceptor) is also a GPCR, which
primarily signals through phospholipase C
stimulation but has a secondary action on
adenylyl cyclase. Vasopressin is a partialagonist
at OT but its effects are limited by the
distribution of the receptor, which, as might be
inferred from its classic action on the pregnant
uterus, is high in the myometrium, endometrium,
mammary gland and ovary.
2. Action of oxytocin onmyometrium is independent of
innervation. Thereare specific G-protein coupled
oxytocin receptorswhich mediate the response
mainly by depo-larization of muscle fibres and
influx of Ca2+ ions as well as through
phosphoinositide hydrolysisand IP3 mediated
intracellular release of Ca2+ ions.The number of
oxytocin receptors increasesmarkedly during later
part of pregnancy. Oxytocinincreases PG synthesis
and release by theendometrium which may
contribute to thecontractile response. Distinct
subtypes of oxytocinreceptors have been shown
on the myometriumand the endometrium.

4. Thyroid Gland 1. Thyroxin(T4)or
Tetraiodothyronine &
Triiodothyronine(T3)
2. Calcitonin
1. Both T3 and T4 penetrate cells by active
transportand produce majority of their actions by
combiningwith a nuclear thyroid hormone receptor
(TR)which belongs to the steroid and
retinoidsuperfamily of intracellular receptors. In contrast
to the steroid receptor, the TRresides in the nucleus
even in the unligandedinactive state. It is bound to
the ‘thyroid hormoneresponse element’ (TRE) in the
enhancer regionof the target genes along with
corepressors.When T3 binds to the ligand-binding
domain ofTR, it heterodimerizes with retinoid X
receptor(RXR) and undergoes a conformation
changereleasing the corepressor and binding
thecoactivator. This induces gene transcription
→production of specific mRNA and a specificpattern
of protein synthesis → various metabolicand anatomic
effects.
2. The actions of calcitonin are mediated througha G-
protein coupled calcitonin receptor (CTR)and
increase in cAMP formation, but its targetcells are
different from that of PTH.
Parathyroid Gland  Parathyroid Hormone(PTH)  The PTH receptor is a G protein coupled receptor
which on activationincreases cAMP formation and
intracellular Ca2+in target cells. In bone, the target
cell is the osteo-blast because PTH receptors are not
expressedon the surface of osteoclasts. Acting on
theosteoblast, PTH induces a factor ‘Receptor
foractivation of nuclear factor-κB-ligand’
(RANKL)which diffuses and combines with RANK
onosteoclast precursors and transforms them
intoosteoclasts as well as activates osteoclasts
(Fig.24.2). In addition, birth rate of bone
remodelingunits into which osteoclasts are recruited
isenhanced. Formation of the remodeling pit isfollowed
by osteoblastic deposition of new boneinto it. PTH
enhances proliferation anddifferentiation of preosteoblasts
and depositionof osteoid as well. Bone resorption
predominateswhen high concentrations of PTH are
presentcontinuously, but intermittent exposure to
lowconcentrations has the opposite effect.

5. Stomach  Gastrin  Gastrin binds to cholecystokinin B receptors to
stimulate the release of histamines in
enterochromaffin-like cells, and it induces the
insertion of K+
/H+
ATPase pumps into the
apical membrane of parietal cells (which in
turn increases H+
release into the stomach
cavity).
Small Intestine 1. Secretin
2. Cholecystokinin(CCK)
1. Human secretin is a ligand at G-protein coupled
secretin receptors which are expressed in the
basolateral domain of several tissue cell types,
including pancreas, stomach, liver, colon and other
tissues. Upon interaction, levels of cAMP increase
and initiates the cAMP-mediated signalling cascade
that results in phosphorylation of protein kinase A
(PKA) and activation of cystic fibrosis
transmembrane conductance regulator (CFTR).
Activation of CFTR activates Cl-/HCO3- anion
exchanger 2 and leads to secretion of bicarbonate-
rich-pancreatic fluid. Via the same cAMP signalling
pathway, secretin promotes the secretion of water
and electrolytes in cholangiocytes.
2. Receptor occupancy leads to phosphotidylinositide
breakdown and Ca2+ mobilization. Recent studies
with the fluorescent chelate probe Quin-2 have
shown that CCK increases cytosolic Ca2+ from a
basal level of 100 nM to 500 approximately 1000
nM. The effects of Ca2+, and diacylglycerol
produced by the breakdown of phosphoinositides, are
believed mediated by activation of a group of protein
kinases and phosphatases. It stimulates the acinar
cells of the pancreas to release a juice rich in
pancreatic digestive enzymes (hence an alternate
name, pancreozymin) that catalyze the digestion of
fat, protein, and carbohydrates.
Pancreas 1. Insulin(β cells) 1. The binding of insulin to the alpha subunit of IR
stimulates the tyrosine kinase activity intrinsic to the
beta subunit of the receptor. The bound receptor is
able to autophosphorylate and phosphorylate
numerous intracellular substrates such as insulin
receptor substrates (IRS) proteins, Cbl, APS, Shc
and Gab 1. These activated proteins, in turn, lead
to the activation of downstream signaling molecules
including PI3 kinase and Akt. Akt regulates the
activity of glucose transporter 4 (GLUT4) and
protein kinase C (PKC) which play a critical role in
metabolism and catabolism. Insulin stimulates glucose
transport across cell membrane by ATP dependent
translocation of glucose transporter GLUT4 to the
plasma membrane.

6. 2. Glucagon(α cells) 2. Glucagon binds to the glucagon receptor activating
Gsα and Gq. This activation activates adenylate
cyclase, which increases intracellular cyclic AMP and
activates protein kinase A. Activating Gq activates
phospholipase C, increases production of inositol
1,4,5-triphosphate, and releases intracellular
calcium. Protein kinase A phosphorylates glycogen
phosphorylase kinase, which phosphorylates glycogen
phosphorylase, which phosphorylates glycogen,
causing its breakdown.
Adrenal gland
(cortex)
1. Glucocorticoids
2. Mineralocorticoids(principally
aldosterone)
1. The glucocorticoid effects are initiated by interaction of
the drugs with specific intracellular glucocorticoid
receptors belonging to the nuclear receptor superfamily.
This superfamily also includes the receptors for
mineralocorticoids, the sex steroids, thyroid hormones,
vitamin D3 and retinoic acid. The actual mechanism of
transcriptional control is complex, with atleast four
mechanisms operating within the nucleus.
2. Aldosterone acts through specific intracellular receptors
of the nuclear receptor family. Unlike the glucocorticoid
receptor, which is present in most cells, the
mineralocorticoid receptor is restricted to a few tissues,
such as the kidney and the transporting epithelia of
the colon and bladder. Cells containing
mineralocorticoid receptors also contain the 11β-
hydroxysteroid dehydrogenase type 2 enzyme, which
converts hydrocortisone(cortisol) into inactive cortisone,
but does not inactivate aldosterone. The interaction of
aldosterone with its receptor initiates transcription and
translation of specific proteins, resulting in an increase
in the number of sodium channels in the apical
membrane of the cell, and subsequently an increase in
the number of Na+-K+ ATPase molecules in the
basolateral membrane, causing increased K+ excretion.
In addition to the genomic effects, there is evidence
for a rapid nongenomic effect of aldosterone on Na+
influx, through an action on the Na+-H+ exchanger in
the apical membrane.
Adrenal gland
(medulla)
1. Epinephrine
2. Norepinephrine
1. Epinephrine acts on alpha and beta-adrenergic
receptors. Important effects of epinephrine include
increased heart rate, myocardial contractility, and renin
release via beta-1 receptors. Beta-2 effects produce
bronchodilation.
2. Norepinephrine functions as a peripheral vasoconstrictor
by acting on α adrenergic receptors. It is also an
inotropic stimulator of the heart and dilator of coronary
arteries as a result of it's activity at the β adrenergic

7. receptors.
Testes(male)  Testosterone  The androgen receptor exists in the cytoplasm bound
to the heat shock proteins HSP90, HSP70, and other
chaperones. After binding to an androgen, the
androgen receptor dissociates from HSP90 and
undergoes a conformational change to slow the rate of
dissociation from the androgen receptor. The
androgen-receptor complex is transported into the
nucleus where it binds to DNA and recruits other
transcriptional regulators to form a pre-initiation
complex and eventually induce expression of specific
genes. Testosterone antagonizes the androgen receptor
to induce gene expression that causes the growth and
development of masculine sex organs and secondary
sexual characteristics.
Ovary(female) 1. Estrogen(Estradiol)
2. Progesterone
1. Estradiol works by binding to subtypes of the estrogen
receptor: estrogen receptor alpha (ERα) and estrogen
receptor beta (ERβ). It also exerts potent agonism of
G Protein-coupled estrogen receptor (GPER), which
is recognized an important regulator of this drug's
rapid effects. Once the estrogen receptor has bound
to its ligand, it enters the nucleus of the target cell,
regulating gene transcription and formation of of
messenger RNA. This mRNA makes contact with
ribosomes producing specific proteins that express the
effect of estradiol upon the target cell.
2. Progesterone receptor (PR) is a member of the
nuclear/steroid hormone receptor (SHR) family of
ligand-dependent transcription factors that is expressed
primarily in female reproductive tissue as well as the
central nervous system. The PR exists in a short
(PR-A) and a longer (PR-B)isoforms. The two
have differing activities, but because theligand binding
domain of both is identical, all agonists andantagonists
display similar binding properties for them. As a result
of its binding its associated steroid hormone,
progesterone, the progesterone receptor (PR)
modulates the expression of genes that regulate the
development, differentiation, and proliferation of target
tissues. Progesterone also acts on cell
membranereceptors in certain tissues and produces
rapid effects, likeCa2+ release from spermatozoa and
oocyte maturation,