Hypothalamus and Pituitary

Figure 11-3: Autonomic control centers in the brain

 Hypothalamus

• Integrates functions that maintain chemical

and temperature homeostasis

• Functions with the limbic system

• Controls the release of hormones from the

anterior and posterior pituitary
 Hypothalamus

• Synthesizes releasing hormones in cell bodies of

neurons

• Hormones are transported down the axon and

stored in the nerve endings

• Hormones are released in pulses

 Hypothalamic Releasing Hormones

Seven releasing hormones are made in the

hypothalamus
– Thyrotropin-releasing hormone (TRH)
– Corticotropin-releasing hormone (CRH)
– Gonadotropin-releasing hormone (GnRH)
– Growth hormone-releasing hormone (GHRH)
– Growth hormone-release inhibiting hormone (GHIH)
– Prolactin-releasing factor (PRF)
– Prolactin-inhibiting hormone (PIH)
 Hypothalamus Releasing Hormones:
Secretion

• Is influenced by emotions
• Can be influenced by the metabolic state of
the individual
• Delivered to the anterior pituitary via the
hypothalamic-hypophyseal portal system
• Usually initiates a three-hormone sequence
 Anterior Pituitary

Is also called the Adenohypophysis

Secretes tropic hormones in a pulsatile fashion

Synthesizes various hormones in various specific cell

populations
Gross View
 Anterior Pituitary Hormones

Each of anterior pituitary hormone is synthesized

by a cell population.
Corticotropes - ACTH
Lactotropes - Prolactin
Somatotropes - GH
Thyrotropes - Thyrotropin
Gonadotropes - FSH, LH
 Anterior Pituitary Hormones

Growth Hormone (GH, Somatotropin): primary

hormone responsible for regulating body growth, and is
important in metabolism

Thyroid-stimulating Hormone (TSH): stimulates

secretion of thyroid hormone & growth of thyroid gland

Adrenocorticotropic Hormone (ACTH): stimulates

cortisol secretion by the adrenal cortex & promotes
growth of adrenal cortex
 Anterior Pituitary Hormones

Follicle-stimulating Hormone (FSH): Females:

stimulates growth & development of ovarian follicles,
promotes secretion of estrogen by ovaries.
Males: required for sperm production
Luteinizing Hormone (LH): Females: responsible for
ovulation, formation of corpus luteum in the ovary, and
regulation of ovarian secretion of female sex hormones.
Males: stimulates cell in the testes to secrete testosterone
Prolactin: Females: stimulates breast development and
milk production. Males: involved in testicular function
HYPOTHALAMIC EFFECTS ON THE
HORMONE ANTERIOR PITUITARY
Thyrotropin-releasing hormone Stimulates release of TSH
(TRH) (thyrotropin) and Prolactin
Corticotropin-releasing hormone Stimulates release of ACTH
(CRH) (corticotropin)
Gonadrotropin-releasing Stimulates release of FSH and
hormone (GnRH) LH (gonadotropins)
Growth hormone-releasing Stimulates release of growth
hormone (GHRH) hormone
Growth hormone-inhibiting Inhibits release of growth
hormone (GHIH) hormone
{Prolactin-inhibiting hormone Stimulates release of prolactin
(PIH)
Prolactin-inhibiting hormone Inhibits release of prolactin
(PIH)
 Growth Hormone Activity

Increases plasma free fatty acids (FFA) - source of

energy for muscle tissue

Increases hepatic glucose output

Decreases insulin sensitivity in muscle

Is protein anabolic hormone

 Growth Hormone Activity

Exerts its growth-promoting through interactions

[mainly induction of Insulin-like Growth Factor I (IGF-
I)].

IGF-I synthesis is stimulated by GH

Major source of IGF-I is the liver; IGF-I is also locally

produced in other tissues
 Endocrine Control: Three Levels
of Integration

• Hypothalamic stimulation–from CNS

• Pituitary stimulation–from hypothalamic trophic Hs
• Endocrine gland stimulation–from pituitary trophic Hs
Endocrine Control: Three Levels
of Integration

Figure 7-13: Hormones of the hypothalamic-anterior pituitary pathway

 Multiple Stimuli for Hormone
Release:
Nervous & Endocrine
• Stimuli
– Stretch
– Glucose
– Insulin levels
• Reflex
– Lower blood glucose
– Reduces stimulus
– Reduces insulin release
 Multiple Hormones Can Target a
Cell/Tissue
• Growth Hormone
• Somatomedins
• Thyroxin
– All have receptors
on many tissues
– Stimulate pathways
for growth

Figure 7-17: A complex endocrine pathway

 More Impacts on Target Cells
• Synergism: multiple stimuli more than additive
– Cortisol +5
– Glucagon +10
– Epinephrine +20 (added = +35)
– Synergistic effect + 140
• Antagonism: glucagons opposes insulin
• Permissiveness: need 2nd hormone to get full
expression
More Impacts on Target Cells

Figure 7-18: Synergism

 Posterior Pituitary
Comprised of the endings of axons from cell bodies in
the hypothalamus (supraoptic and paraventricular)

Axons pass from the hypothalamus to the posterior

pituitary via the hypothalamohypophysial tract

Posterior pituitary hormones are synthesized in the

cell bodies of neurons in the supraoptic and
paraventricular nuclei
 Posterior Pituitary

Hormones synthesized in the hypothalamus are

transported down the axons to the endings in the posterior
pituitary

Hormones are stored in vesicles in the posterior pituitary

until release into the circulation

Principal Hormones: Vasopressin & Oxytocin

Secretion of Posterior Pituitary
Hormones

Figure 7-12: Synthesis, storage, and release of posterior pituitary hormones

 Oxytocin

Is synthesized as the precursor hormone: prepro-

oxyphysin

Acts primarily on the mammary gland and uterus

Increases contraction of smooth muscle of the vas

deferens
 Oxytocin

Secretion is increased during labor

May also act to facilitate sperm transport in uterus

(non-pregnancy state)
 Posterior Pituitary: Regulation of Osmolality

Plasma osmolality is monitored by osmoreceptors in the

hypothalamus

Increases in plasma osmolality stimulates secretion of

vasopressin

Small changes above the normal plasma osmotic pressure

(285 mosm/kg) stimulate release of vasopressin
 Vasopressin (ADH)

Is also known as antiduretic hormone (ADH)

Participates in body water regulation (Water is lost

from lungs, sweat, feces and urine on a daily basis)
 Osmolality

• Refers to the amount of solutes in a solution

• Loss or gain of water without solutes (free water

gain or loss) changes the osmolality of ECF

• Must be regulated to maintain normal cell activity

 Vasopressin (ADH) Secretion

Secretion is Stimulated by:

1. Large decreases in blood volume
2. Decreases in blood pressure
3. Pain, fear, trauma, and stress
 Vasopressin Activity

Decreases water excretion by kidneys (V2 receptors)

Constricts blood vessels (V1 receptors)- arteriolar smooth

muscle

Increases adrenocorticortropin hormone (V1B receptors)

secretion from the anterior pituitary
 AVP and Water Balance

• The maintenance of water balance in the body is

extremely important for proper functioning of
cells.
• There are two main compartments of the body:
intracellular and extracellular (includes interstitial
space and plasma).
• Water moves freely between compartments
depending upon osmotic gradients.
 Osmolarity and Osmosis

• The osmolarity of a solution is determined by how much

solute (such as salt) is present in a given amount of solvent
(such as water).
• Water will move by osmosis from an area of lower
osmolarity to one of higher osmolarity.
• Which way will water move in this example?
semipermeable membrane
(cell membrane)
 The Main Point....

• If there is insufficient fluid in the extracellular space,

osmolarity increases, and water will begin to leave
cells.
• This is a bad thing to have happen, cells will not be
happy!
• One must regulate the amount of water in the body.
 The Role of the Kidney in Water Balance

• The kidney removes about 170 liters/day of water

from the blood.
• 99% of this water is reabsorbed from the urine back
into the bloodstream.
• The kidney is an important site at which the water
content of the body is regulated.
 AVP and Water Balance
 Old name: antidiuretic hormone (ADH) From where?
 Synthesized in the brain (what part?), released from
posterior pituitary.
 Stim by hypo-osmotic neurons in response to incr
osmolarity of blood or decr blood vol., and by pain,
some drugs, low bp.
 Action: increases permeability of the distal convoluted
tubule and collecting ducts to water
 Result:
- increased water reabsorption from urine
- decreased urine volume
- decreased osmolality of interstitial fluids
- increased blood pressure
 Regulation of AVP Secretion

 Response to osmolality of interstitial fluid:

- Osmoreceptors in the brain detect changes in
osmolality of the interstitial fluid or blood.
- Increased osmolality results in increased [solutes]
AVP release
- increased water reabsorption
- decreased osmolality of fluids
- Decreased osmolality results in decreased ADH
release = NEGATIVE FEEDBACK!
- decreased water reabsorption
- increased osmolality of fluids
 Regulation of AVP Secretion

 Response to changes in blood pressure:

- Blood pressure receptors in heart, aortic arch, and
carotid artery
- Increased blood pressure results in decreased AVP
release
- decreased water reabsorption
- decreased blood volume, blood pressure
- Decreased blood pressure results in increased AVP
release
- increased water reabsorption
- increased blood volume, pressure
 Regulation of AVP Secretion
 AVP release is also inhibited by alcohol, caffeine
(diuretics) – dehydrating effect “dry mouth” or intense
thirst morning after  INCREASED urine output.
- decreased water reabsorption
- increased urinary volume
- potential for dehydration
Some drugs can also antagonize ADH release: diuretics used
to treat high bp, edema, or CHF.
 Insufficient AVP results in disease: diabetes insipidus
(DI)
- impaired water reabsorption from DCT, collecting ducts
- increase urine volume 10 times and intense thirst.
DI can be caused by a blow to the head or other
hypothalamic damage.
Feedback
mechanisms in the
control of blood
osmotic pressure—
the control of ADH.
Feedback control of Endocrine Secretion
Feedback control of Endocrine Secretion
The Hypophyseal Portal System
Negative Feedback Controls: Long and Short Loop
Reflexes
Negative Feedback Controls: Long and Short Loop
Reflexes
 Pathologies: Over or Under
Production
• "no bad hormones – just too much or too little"
• Exogenous medication
– Replaces & exceeds normal
– Cause atrophy of gland
• Hypersecretion: too much
– Tumors or cancer
– Grave's disease- thyroxin
• Hyposecretion: too little
– Goiter – thyroxin
– Diabetes – insulin
Pathologies: Over or Under
Production
 Pathologies: Due to Receptors

• Downregulation – hyperinsulinemia
• Transduction abnormalities
– Testicular feminization syndrome
– Pseudohypothyroidism
• Abnormalities of control mechanisms
Pathologies: Due to Receptors

Figure 7-20: Primary and secondary hypersecretion of cortisol