BASIC ENDOCRINE MECHANISMS
Joel Michael, PhD
Department of Molecular Biophysics and Physiology
Levy, Koeppen, Stanton, Principle of Physiology, 4th edition, Chapter 41
The student should be able to:
1. define hormone, receptor, target cell.
2. distinguish endocrine, paracrine, neuroendocrine and synaptic chemical
3. list the three chemical classes of hormones.
6. describe the processes that determine the concentration of a circulating
7. describe the feedback regulation of hormone secretion using specific
8. predict the results of disturbances to an endocrine feedback system
occurring any where in the system.
9. describe the importance of pulsatile and diurnal secretion of hormones.
10. describe the steps in the actions of steroid hormones mediated by binding to
11. describe the steps in the actions of peptide hormones mediated by binding
to fixed receptors
12. define and give examples of direct and permissive actions of hormones.
13. define the trophic effect of a hormone.
14. define antagonistic and synergistic effects of two hormones.
15. describe common causes of hypo- and hypersecretion of hormones and
predict the consequences of each for any hormone.
16. describe the anatomical relationship between the hypothalamus and the
pituitary, and the functional significance of this relationship.
17. describe the structure and the significance of the hypothalamico-
hypophyseal portal system.
18. list the hormones released by the posterior pituitary, the mechanisms
controlling their release, and their peripheral functions.
19. describe the feedback control of hormone secretion at all three levels of the
hypothalamic-pituitary-target organ axis.
“extranuclear” negative feedback systems
amines hormones permissive effect
antagonistically posterior pituitary
anterior pituitary protein hormones
cell membrane pulsatile
chemical messengers receptors
diurnal second messengers
dose-response short loop feed back
ductless steroids hormones
endocrine glands synergistically
enzymes target cell
fixed receptors target cells
half-life the hypothalamic-pituitary-target organ
hypothalamus transport proteins
intranuclear receptors trophic effects
long loop feedback up and down-regulation
I. Endocrine Systems: An Overview (FIG. 1)
A. Endocrine glands are identifiable groups of cells that manufacture and
secrete specific chemical messengers called hormones.
B. Hormones are chemical messengers that circulate in the blood and alter
the function of all those cells (target cells) possessing receptors for that
C. Target cells possess receptors which bind the hormone, resulting in
altered behavior of the cell (the response).
II. Endocrine Glands:
A. are capable of synthesizing and releasing hormones in response to
B. are ductless, and the hormones they release either diffuse to neighboring
target cells or diffuse into capillaries and are carried throughout the body
by the circulation.
C. may require the presence of a trophic substance to maintain their integrity
D. A list of the endocrine glands we will be considering and their hormones
can be found in Figure 1-2 (FIG. 2)
III. Basic Properties of Hormones
A. Hormones control or determine the activity of target cells at a distance.
They are one example of cell-cell communications.
B. Hormones carry information that cause target cells to alter their function
1. Hormones are not themselves enzymes, although they ultimately alter
enzyme levels and/or activity in their target cells.
Endocrine systems and the ways in which they exert their effects on target cells.
NOTE: (1) hormone must bind to receptor to produce any effect and (2) the
physiological effect arises from changes in intracellular enzyme activity.
(3) Every cell has receptors for many different hormones each of which
simultaneously contributes to determining cell function.
ENDOCRINE HORMONE EFFECTS
Hypothalamus Thyrotropin releasing hormone (TRH) Stim. TSH release
Corticotropin releasing hormone (CRH) Stim. ACTH release
Gonadotropin releasing hormone (GnRH) Stim. FSH & LH release
Growth hormone releasing hormone (GHRH) Stim. GH release
Growth hormone inhibiting hormone (GHIH) Inhibits GH release
Prolactin releasing hormone (PRH) Stim. prolactin release
Prolactin inhibiting hormone (PIH) Inhibits prolactin release
Anterior pituitary Thyroid stimulating hornone (TSH) Stim. T3/T4 synth./rel.
Adrenocorticotropic hormone (ACTH) Stim. cortisol release
Growth hormone (GH) Stim. somatomedin release
from liver; significant effects
Follicle stimulating hormone (FSH) Stim. follicle growth and
Luteinizing hormone (LH) Stim. ovulation and ovarian
estradiol and progesterone
Prolactin Stim. milk production
Posterior pituitary Vasopressin (antidiuretic hormone-ADH) Stim. renal reaborption of
Oxytocin Stim. milk secretion and
Thyroid gland Tetraiodothyronine (thyroxin = T4) Precursor form of T3
Triiodothyronine (T3) Stim. growth, different-iation,
Thyroid gland Calcitonin (CT) Decreases plasma [Ca ]
Adrenal cortex Aldosterone Stimulates Na retention by
Cortisol Increased carbohydrate
metabolism (blood glucose
Androgens Reproductive function
FIGURE 2 (continued on next page)
ENDOCRINE GLAND HORMONE EFFECTS
Adrenal medulla Epinephrine/Norepinephrine Many stimulatory/inhibitory effects on
nerves, glands, smooth muscle
Pancreas (islets) Insulin ($-cells) Decrease blood glucose concentration
Glucagon ("-cells) Increases blood glucose concentration
Somostatin (D-cells) Decrease secretion of other islet
Parathyroid Parathyroid hormone (PTH) Increases blood [Ca ]
Ovaries Estrogen Stimulate female sexual development
Progersterone Increase uterine and mammary gland
Inhibin Decreases FSH secretion
Testes Testosterone Increases male sexual development and
Inhibin Decreases FSH secretion
Placenta Estrogen Stimulation of uterine and breat growth
Chorionic gonadotropin Increases progesterone synthesis by
Skin Vitamin D Increases blood [Ca ]
Liver Somatomedin (=IGF-1) Stimulates growth
FIGURE 2 (continued)
A list of the major endocrine glands, the hormones that are released by the
endocrine cells, and the major physiological effects of these hormones (generally
very much simplified). We will discuss these hormones in different blocks
throughout the year. DO NOT MEMORIZE! Source: JAM
IV. Chemical Nature of Hormones (FIG. 3)
A. Protein hormones are made of 50 or more amino acids, while peptide
hormones have fewer than 50 amino acids.
1. Synthesis of preprohormone occurs in ribosomes on the rough
2. Prohormone cleaved off in the Golgi apparatus.
3. Hormone packaged in secretory vesicles for storage.
4. Hormone release occurs from vesicles.
B. Steroids hormones are ALL synthesized from cholesterol
1. Cells take up low-density lipoprotein (LDL) and make cholesterol
2. There is a complex pathway by which the steroid hormones can be
3. Steroid hormones are not stored, but are released as they are
4. The similarity of the chemical structures of cortisol and aldosterone
C. Amines hormones are derived from tyrosine
1. They are synthesized either in specialized extracellular
compartment (thyroid hormone) or via enzymes in the cytosol
2. They are stored and secreted on demand.
CHEMICAL HORMONE # OF AAs MAJOR SOURCE
Peptides & Proteins ADH (vasopressin) 9 Posterior pituitary
GnRH 10 Hypothalamus
TRH 3 Hypothalamus
Somatostatin 14 Hypothalamus &
Insulin 55 Pancreas (-cells)
Glucagon 29 Pancreas (-cells)
Growth hormone 191 Anterior pituitary
Prolactin 198 Anterior pituitary
PTH 84 Parathyroid
Calcitonin 32 Thyroid (C cells)
ACTH 39 Anterior pituitary
Somatomedin (IGF-1) 70 Liver, bone
Glycoproteins FSH Anterior pituitary
LH Anterior pituitary
Chorionic gomadotropin Placenta
TSH Anterior pituitary
Steroids Estrogen Ovaries, placenta
Progesterone Corpus luteum, placenta
Glucocorticoids Adrenal cortex
Aldosterone Adrenal cortex
Vitamin D metabolites Liver, kidneys
Amines Dopamine CNS
Epinephrine/norEpi Adrenal medulla
Thyroid homrones Thyroid
Chemical classification of hormones. Peptides have fewer than 50 amino acids,
while protein hormones have 50 or more. DON’T MEMORIZE!
V. Transport of hormones in the blood
A. Protein and peptide hormones, and the amine hormones dopamine and
epinephrine, are water soluble and hence are carried in plasma as simple
C. Steroid hormones and thyroid hormone have a very low solubility in water
and are carried in the blood bound to specific plasma protein transporters.
1. These transport proteins are made in the liver and their production
is determined by and can be altered by metabolic and endocrine
2. Some transport proteins only bind a specific hormone, while others
3. Only the small percentage of the transported hormones is present
unbound and in solution in the plasma, but it is only the unbound
hormone that is free to diffuse to its target cells. Thus, only
the unbound hormone is biologically active.
4. Changes in the concentrations of these transport proteins can thus
affect hormone activity.
Transport protein Hormone transported
CBG (transcortin) Corticosteroids (cortisol)
TGB (thyroxine-binding globulin) T3/T4
SHBG (sex hormone-binding Testosterone, estrogen
Albumin Steroid hormones (non-specific)
Prealbumin (transthyretin) T4 (and other biologically active substances)
Many different plasma proteins IGF-1 (somatomedin)
Plasma proteins involved in transporting non-soluble hormones (steroids and
thyroid hormone) to their target cells. These proteins are manufactured in the
liver. (Note that there are other transport proteins carrying other hormones; see
Section 2). Source: JAM
VI. Determinants of Free, Active Hormone Concentration (FIG. 5)
A. Rate of release from secretory cell is often determined by negative
B. Binding to transport proteins (if any are involved); steroid hormones and
thyroid hormone are transported bound to plasma proteins
C. Binding to target cell receptors
D. Degradation in liver and other peripheral tissues and excretion in urine or
1. Rate of removal from circulation referred to as the half-life
The concentration of free
hormone in the plasma is
determined by the rate of
release (secretion), binding to
plasma proteins (if transport
proteins are involved),
metabolism (degradation) and
elimination (in urine or feces),
and binding to receptor proteins.
NOTE: hormones must bind
to a receptor to alter cell
function. Physiologically, the
concentration of free
hormone (and hence the
probability of binding to a
receptor) is altered by
changing the rate of secretion
(altering the stimuli that affect
the endocrine cell).
Amines A few minutes
T4 As long as one week
T3 A day or less
Polypeptides As long as 2/3 hour
Proteins As long as 3 hours
Steroids Up to 2 hours
The half-life (the time for half of the content of a hormone to be
removed from the circulation) of the different classes of hormones.
NOTE: the half-lives of hormones range from minutes to a week.
TAKE HOME MESSAGE
The concentration of free hormone determines the probability of binding to a
cellular receptor. The principal physiological determinant of hormone
concentration is the rate of release of the hormone from the endocrine cell in
which it is made.
VII. Control of Hormone Release From Endocrine Cells Is Determined By Different
A. Some physiological stimulus acting on secretory cell (for example, [K],
[glucose], [Ca] etc.) (FIG. 7)
B. Some other hormone acting on the secretory cells (FIG. 8)
C. Neural inputs (action potentials generated) to secretory cells (which are
neurons) trigger the release of hormone. (FIG. 9)
One example of an endocrine system (one that regulates blood glucose) where
the stimulus for hormone (insulin) release is some physiological parameter (here
the plasma concentration of glucose) acting on the secretory cell (the beta cells).
NOTE: This is, of course, a classical negative feedback system (regulating
blood glucose). Source: JAM.
A model of an endocrine system in which a number of hormones, acting on
different secretory cells (in hypothalamus, pituitary and adrenal gland) determine
the rate of hormone secretion and hence the biological response. NOTE: This is
also a classical negative feedback system, although obviously a more
complex one than the system illustrated in Figure 1-12.
Source: Devlin, Figure 23.2.
TAKE HOME MESSAGE
The rate of secretion of a hormone is almost always determined by a
negative-feedback system of some kind.
Neural inputs to secretory cells can cause release of hormones such as ADH and
epinephrine. Source: JAM
D. In addition to the effects of other stimuli determining the rate of release of
hormones, there are “clock-like” inputs to endocrine cells that produce
temporal variations in the rate of release.
1. Pulses of gonadal hormones result from the pulsatile
(approximately two/hour) release of hormones all along the
controlling axis (FIG. 10)
2. Diurnal rhythm (24-hour clock) of release is visible in changing
levels of ACTH and cortisol (FIG. 11)
(2/hour approximately) of
peripheral vein plasma
LH concentration and
portal vein plasma LHRH
concentration (in female
sheep, but a similar effect
is known to occur in
women). Each pulse of
LHRH is responsible for
producing a pulse of LH.
Source: Berne and Levy,
Diurnal rhythm of cortisol secretion; plasma cortisol is at its highest level around
8 a.m. NOTE: It is therefore essential that any assessment (for example, for
purposes of diagnosis) of cortisol levels (or any other hormones exhibiting
a diurnal rhythm) be done at the same time of day. Cortisol is normally
measured at 8 a.m. Source: Berne and Levy, 1993
VIII. Mechanism of Action at Target Cell
A. For a hormone to alter the function of a cell, there must be receptors for
that hormone in or on the cell.
B. Fixed receptors are located on the cell membrane: protein/peptide,
dopamine, and the catecholamines all bind to cell membrane receptors.
1. Hormones binding to membrane receptors activate a variety of
intracellular second messengers that ultimately alter cell function by
altering the activity of intracellular enzymes.
C. Mobile receptors are present within the cell: steroid hormones andthyroid
hormones bind to intranuclear receptors (and some also bind to receptors
in the cytosol).
1. The “classical” model asserted that steroid hormones act only by
entering the nucleus and altering gene expression to alter the
production of enzymes (proteins). (FIG. 13)
2. However, there is now clear that at least some steroid hormones
also have “extranuclear” effects that result from their altering
cytosolic second messenger systems which can alter existing
enzyme activity (which produces rapid changes in cell function).
The consequences of hormone binding to extranuclear receptors
can also affect gene expression. (FIG. 14)
D. Every target cell (and that means every cell in the body) has receptors
(membrane and intracellular) for a great many different hormones some
of which act on the same cellular functions. The interactions between the
hormones can be very complex. (FIG. 15)
TAKE HOME MESSAGE
Hormones bind to either fixed, membrane bound receptors or to mobile,
intracellular receptors. Binding of the hormone to its receptor triggers a
cascade of events that ultimately lead to alterations in cellular enzyme
activity. Cells have receptors for many different hormones.
Binding of signaling hormones (protein, peptides, epinephrine/norepinephrine.) to
membrane receptors can activate a wide variety of intracellular signaling
mechanisms all of which ultimately alter enzyme activity. This results in the
biological response of the target cell.
Source: Levy, Koeppen, Stanton, Figure 5-1
The “classical” model of the mechanism of action of lipid soluble hormones
steroids, vitamin D, thyroid hormone). The hormone molecules enter the
cytoplasm where some bind to cytoplasmic receptors. The receptor-hormone
complex diffuses into the nucleus. Some hormone molecules diffuse directly
into the nucleus where they bind to receptors. In the nucleus, transcription and
translation are altered, resulting in a change in the production of enzymes
(proteins) and the generation of a biological response.
Source: Devlin, Figure 23.48
A model for the dual mechanism by which a steroid hormone like estrogen and,
it is believed, other steroid hormones produce their effects. (1) The “classical”
nuclear effect Involves estrogen diffusing into the cell and then into the nucleus
where it binds to a receptor. The result is alter gene expression
(transcription/translation) and altered enzyme activity in the cell. Cell function is
then changed. (2) There is also a non-nuclear (“non-genomic”) action that
involves estrogen binding to a cytosolic receptor and thus activating a cascade of
second messengers to alter enzyme activity. (3) Note that it is likely that some
of those second messengers are thought to also alter gene expression in the
Drawing by JAM
B. J. Cheskis, Regulation of cell signalling cascades by steroid hormones.
Journal of Cellular Biochemistry, 93, 20-27, 2004.
Cells have receptors for many chemical messengers and hormones. When the
receptor binds its ligand complex metabolic pathways are activated altering cell
function in a myriad of ways, often using the same reaction pathways. Multiple
the situation illustrated here and you can image the complexity involved in
understanding how endocrine mechanisms affect any particular function (for
example, regulation of blood glucose). Source: Devlin, Fig. 13.34.
IX. Actions of Hormones on Target Cells
A. Dose-response relationship defines the relationship between the
concentration of a hormone and the magnitude of the response (however
measured) that results. (FIG. 16)
1. The maximum response can be measured, and expressed as some
number of units of measure, or it can be expressed as a percentage of some
defined maximal response.
2. Sensitivity is defined as the hormone concentration that is required
to produce 1/2 the maximum response
3. Maximum responsiveness can be decreased from normal levels by
such perturbations as decrease in the total number of functional
target cells, decrease in the number of receptors on each cell,
intracellular changes in enzymes etc.
4. Sensitivity can be decreased by a decrease in the number or
affinity of the receptors, increase in the rate of hormone breakdown
B. Up and down-regulation of receptor number (decreased hormone
concentration leads to increased production of receptors by the target cell
and visa versa).
C. Direct effects alters activity of target cells. (FIG. 17)
The general shape of the dose-response curve. Alterations in this curve can
take the form of a change in maximal responsiveness (left lower panel) or a
change in sensitivity (right lower panel). Note the presence of a threshold
(hormone concentration must be greater than some value for any measurable
response to be visible) Source: Levy, Koeppen, Stanton, Figure 41-9
An example (do not worry about the details here, they will be discussed later) of
the direct alteration of target cell activity by a hormone. NOTE that insulin
stimulation of cells causes increased uptake of glucose, alteration of
enzymes affecting glucose metabolism, and increased entry of a variety of
electrolytes. Source: Levy, Koeppen, Stanton, Figure 43-7.
D. Trophic effects maintain the metabolic activity of the target endocrine
glands and stimulates release of hormone from these glands.
E. Interactions between hormones can take a number of different forms:
1. Every cell has receptors for a MANY DIFFERENT HORMONES
2. In some cases two or more hormones “work together” to bring
about some biological response and in other cases two
hormones may “work against” each other in determining a
a. One form of interaction is for one hormone to have a
permissive effect on the action of a second hormone; a
threshold concentration of hormone X is required for
hormone Y to have any effect.
b. Two hormones may interact synergistically. For example,
hormone X and Y “work together” to promote some
biological response, often non-linearly. (FIGS. 18 & 19)
c. Two hormones can interact antagonistically; hormone X
and hormone Y have opposite effects on a biological
3. All hormones act by altering the activities of enzymes and hence
altering the rate of metabolic pathways.
4. For any particular biological response, the magnitude of the
response depends on the “summation” of the effects (some positive
and some negative) of the many hormones that can affect the
activities of the enzymes involved in creating that response.
60 FIGURE 18
Units of biological response 50 The concept of
two hormones is
illustrated. Note that
20 in this case neither
hormone alone has a
10 major effect.
Resting A B A+B
An actual example of the synergistic interaction of three hormones: cortisol (C),
epinephrine (E) and glucagons (G). Each of them alone increase blood glucose
levels, but G+E has a larger effect that either alone, and C+G+E has a very much
greater effect. From Eigler, N., Sacca, L., and Sherwin, R. S. (1979). Synergistic
increments of glucagons, epinephrine, and cortisol in dog. Journal of Clinical
Investigation, 23, 114.
X. Endocrine pathophysiology (FIG. 20)
A. Hypo/hypersecretion (relative to "normal"): too little/too much will cause
B. Primary/secondary causes: since the secretion of almost every hormone
is under negative feedback control, often by other hormones, the causes
of hypo/hypersecretion can be at the endocrine tissue of interest (primary)
or at any of the endocrine organs involved in feedback mechanisms
1. Endocrine tumors typically hypersecrete the hormones made by
2. Damage of any sort to an endocrine gland will cause them to
XI. Physiological functions of hormones (FIG. 21)
A. Endocrine systems are involved with the regulation of a number of
important physiological functions that include:
1. maintenance of the internal environment
2. regulation of metabolism (the availability of energy substrates)
3. growth and development
B. You will be studying these endocrine functions in the blocks listed
in Figure 28.
Causes of hypo- or hyper-secretion (and hence hypo- and hyper-function) in the
endocrine system. Altered endocrine function can be caused by dysfunction at
all of these different levels of organization. Source: JAM.
Hormones Effectors controlled Covered in:
Regulation of water
[Na+] aldosterone Kidneys Urogenital block
[K+] aldosterone Kidneys Urogenital block
osmolarity ADH Kidneys Urogenital block
blood and ECF ADH kidneys CV/Resp and
volume ANP Urogenital
[Ca+2] & [PO4-2] parathyroid h. bone, kidneys Musculoskeletal
calcitonin bone block
vitamin D3 GI system
Control of insulin liver, muscle, adipose GI/Metabolism
metabolism glucagon cells for all hormones block
Growth and growth All cells Musculoskeletal
development hormone block
Reproduction LH/FSH male and female Urogenital block
androgens reproductive systems
Endocrine systems play many roles in the regulation and control of physiologic
XII. Organization of the endocrine system: the hypothalamic-pituitary-target organ
A. The pituitary hangs down from the bottom of the hypothalamus
Bob: could expand the anatomy and/or embryo here (FIG. 22)
B. Two distinctly different endocrine systems are found here
1. Neurons making up the paraventricular and supraoptic nuclei in the
hypothalamus have axons that extend through the hypothalamus,
down the pituitary stalk, to the posterior pituitary (a neuro-
a. Axons end in close proximity to blood vessels making up the
b. Hormones entering the blood here travel throughout the
2. Neurons in the hypothalamic-hypophysiotropic area of the
hypothalamus have axons that extend into the vicinity of the
hypophyseal portal circulation
a. The hormones released here are carried by the hypophyseal
portal vessels down the stalk of the pituitary to the anterior
b. In the anterior pituitary these hormones diffuse from the
blood to affect the behavior of anterior pituitary endocrine
cells. Hormones released from the anterior pituitary cells
enter the blood and are carried throughout the body.
C. Since the hypothalamus is part of the central nervous system, it integrates
many neural inputs.
1. It serves as a pathway for "visceral" expression of CNS activity.
2. It co-ordinates
a. the activity of the autonomic nervous system.
b. the activity of the endocrine system.
3. The hypothalamus also provides a means of producing endocrine
responses to stimuli detected by the central nervous system.
D. The hypothalamus is a region of the brain where the blood-brain-barrier is
weak and hence:
1. hormones can get into the cerebrospinal fluid to act on
hypothalamic neurons, and
2. hormones released at the median eminence can move easily into
the capillaries there.
TAKE HOME MESSAGE
The hypothalamus is the interface between the two "information
processing" systems 0f the body: the nervous system and the endocrine
system. Remember, the nervous system codes information by the
frequency of firing action potentials, and the endocrine system codes
information by the concentration of hormone that is present.
A schematic overview of the anatomic and functional relationships between the
hypothalamus and the pituitary gland. Note that the posterior pituitary is an
extension of neural tissue that stores neurohormones produced in the
hypothalamus and it has its own arterial blood supply. In contrast the anterior
pituitary is endocrine tissue with a blood supply derived from veins that first drain
neural tissue in the median eminence (a portal circulation). NOTE: By this
arrangement the endocrine cells in the anterior pituitary are exposed to
high concentrations of neurohormones originating in the hypothalamus
and stored in the median eminence.
Source: Levy, Koeppen, Stanton, Figure 45-1.
D. The release of HHH's is controlled by a variety of inputs:
1. neural inputs to the hypothalamus (or signals generated in the
2. hormonal feedback from the anterior pituitary (so-called
short loop feed back; see below).
3. peripheral endocrine glands (so-called long loop feedback; see
E. Some of the HHH's stimulate the release of hormones from their targets in
the anterior pituitary and some inhibit the release of hormones from their
F. Some anterior pituitary cells receive both releasing and inhibiting
hormones from the hypothalamus.
G. There are a number of feedback pathways linking the hypothalamus,
anterior pituitary and target organs. (FIG. 23)
Feedback pathways linking the hypothalamus, anterior pituitary and the target
endocrine organs. Remember, there is not always an ultra-short loop
Source: Redrawn from Levy, Koeppen, Stanton, Figure 45.5.
X111. Hormones of the Anterior Pituitary Bob: This might be the place to talk
about the cells of the pituitary
A. The hormones secreted by the anterior pituitary cells fall into three
1. derivatives of ProOpioMelanoCortin (POMC) (FIG. 24)
a. The secretory cells, corticotrophes, are basophilic.
2. glycoproteins: These peptide hormones are composed of two
chains. (FIG. 25)
a. The alpha chains of all these hormones are the same;
specificity and function is conferred by the beta chains which
b. Thyrotrophes and gonadotrophes are basophilic.
Cleavage of POMC to
yield ACTH and related
Structural similarities among TSH, LH, HCG, and FSH are depicted
schematically. TSH, LH, and FSH are released from the anterior pituitary while
HCG is released from the placenta. Note that all share the same α-subunit.
Source: Berne and Levy, 1993.
3. sommatomammotrophins: These are single chain polypeptides
containing two or three S-S bridges.
a. Somatotrophes and mammotrophes are acidophils.
B. All of the anterior pituitary hormones act via fixed receptors and have both
trophic and stimulatory effects.