power point

1. Hypothalamus and Pituitary

2. Figure 11-3: Autonomic control centers in the brain

3. 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

4. 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

5. 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)

6. 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

7. Anterior Pituitary
Is also called the Adenohypophysis
Secretes tropic hormones in a pulsatile fashion
Synthesizes various hormones in various specific cell
populations

9. Gross View

10. 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

11. 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

12. 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

13. HYPOTHALAMIC
HORMONE
EFFECTS ON THE
ANTERIOR PITUITARY
Thyrotropin-releasing hormone
(TRH)
Stimulates release of TSH
(thyrotropin) and Prolactin
Corticotropin-releasing hormone
(CRH)
Stimulates release of ACTH
(corticotropin)
Gonadrotropin-releasing
hormone (GnRH)
Stimulates release of FSH and
LH (gonadotropins)
Growth hormone-releasing
hormone (GHRH)
Stimulates release of growth
hormone
Growth hormone-inhibiting
hormone (GHIH)
Inhibits release of growth
hormone
{Prolactin-inhibiting hormone
(PIH)
Stimulates release of prolactin
Prolactin-inhibiting hormone
(PIH)
Inhibits release of prolactin

14. 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

15. 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

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

17. Endocrine Control: Three Levels
of Integration
Figure 7-13: Hormones of the hypothalamic-anterior pituitary pathway

18. • Stimuli
– Stretch
– Glucose
– Insulin levels
• Reflex
– Lower blood glucose
– Reduces stimulus
– Reduces insulin release
Multiple Stimuli for Hormone
Release:
Nervous & Endocrine

19. • Growth Hormone
• Somatomedins
• Thyroxin
– All have receptors
on many tissues
– Stimulate pathways
for growth
Multiple Hormones Can Target a
Cell/Tissue
Figure 7-17: A complex endocrine pathway

20. • 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

21. More Impacts on Target Cells
Figure 7-18: Synergism

22. 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

23. 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

24. Secretion of Posterior Pituitary
Hormones
Figure 7-12: Synthesis, storage, and release of posterior pituitary hormones

25. 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

26. Oxytocin
Secretion is increased during labor
May also act to facilitate sperm transport in uterus
(non-pregnancy state)

27. 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

28. 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)

29. 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

30. Vasopressin (ADH) Secretion
Secretion is Stimulated by:
1. Large decreases in blood volume
2. Decreases in blood pressure
3. Pain, fear, trauma, and stress

31. 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

32. 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.

33. 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)

34. 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.

35. 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.

36. 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

37. 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

38. 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

39. 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.

40. Feedback
mechanisms in the
control of blood
osmotic pressure—
the control of ADH.

42. Feedback control of Endocrine Secretion

43. Feedback control of Endocrine Secretion

46. The Hypophyseal Portal System

47. Negative Feedback Controls: Long and Short Loop
Reflexes

48. Negative Feedback Controls: Long and Short Loop
Reflexes

49. • "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

50. Pathologies: Over or Under
Production

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

52. Pathologies: Due to Receptors
Figure 7-20: Primary and secondary hypersecretion of cortisol