a&p ii endocrinology11

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Anatomy & Physiology II-BIO 111Dr. G. Krasilovsky

• Welcome• Home Telephone:

845-735-9098• e-mail: gkrasilo@• sunyrockland.edu• (ATT: BIO 111)• Office hours: before

class in this room

mailto:gkrasilo@%0Dsunyrockland.edu

mailto:gkrasilo@%0Dsunyrockland.edu

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ENDOCRINOLOGY

Marieb and Hoehnth

8th Edition- CHAP. 16

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• I. Introduction– A. 1. Homeostasis

• Self-regulation of internal environment and its life functions within a normal range

– 2. Communication within the organism maintains homeostasis

• a. Nervous System:– Stimulus - change in the environment

– Response - correction/reaction to stimulus

– Sensory Interneuron Motor Effector

• b. Chemicals released by glands

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• 2. b. Chemicals released by glands(group of cells capable of secretion)– 1. Exocrine Glands

• Releases chemicals into a duct which

• opens into a space or cavity or surface

• Sweat glands, Salivary glands

– 2. Endocrine Glands• Ductless glands which release their

• Chemicals/secretions into the blood system

• Adrenal / Pituitary glands

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Exocrine with duct Endocrine / ductless

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3. Comparison:

Nervous System

Endocrine System

•Mode: Electrical signals & Neurotransmitter

Chemicals

•Communication Synapses & Receptors

Circulatory System & Receptors

•Time of Action

Short term & Quick

Longer term since chemical circulates

•Specificity Usually specific & localized

Specific or widespread (Receptors)

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• 4. HORMONE:– Chemical substance produced by a gland

– (group of cells)

– Released into the circulatory system

– In small concentrations (potent) and

– Circulate all over the body, but only affect distant target organs which possess

– Specific receptors for the hormone

• 4. Nerve/brain cells release a chemical not into a synapse, but into the circulatory system– Neuroendocrine cells

– Neurosecretory cells

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Fig. 16.1

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• I. B. Types of Hormones– 1. Modified single amino acids (tyrosine)

• Thyroid hormone: tyrosine + iodine

• Epinephrine & Norepinephrine of adrenal gland

– 2. Small peptides (3-10 a.a. in chain)• Hypothalamic releasing hormones

• Pituitary gland (ACTH, oxytocin)

– 3. Large peptides (over 50 a.a.) = Protein• Pituitary gland (growth hormone & prolactin)

• Pancreas (insulin)

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• I. B. (continued)– 4. Steroids (cholesterol backbone)

• Adrenal cortex (cortisone)

• Gonads (estrogen, progesterone, testosterone)

– 5. Fatty Acids converted into Prostaglandins• Many different prostaglandins

• “local hormone”

• Released and functions in a specific area, does not circulate in the blood as it is destroyed in blood

• Sensitizes an area for another chemical to work

• Aspirin inhibits the synthesis of prostaglandins

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I. C. Cellular Basis of Hormonal Action

• 1. Review Fluid Mosaic Model of the cell membrane and the role of membrane protein receptors (pages 64 - 65)

• 2. Second Messenger – Cyclic AMP

Fig. 3.3 & 3.4

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• I. C. Cellular Basis of Hormonal Action• 2. Second Messenger – Cyclic AMP

– a. amino acid and peptide hormones act as first messenger and binds to membrane receptor on outer surface of cell membrane and via a G protein, activates adenylate cyclase on the inner membrane

– b. adenylate cyclase works in cytoplasm to breakdown ATP to ADP and then to AMP and produces cyclic AMP

– c. cyclic AMP activates a group of enzymes known as protein kinases that phosphorylate proteins, usually enzymes, that are responsible for a specific physiological response. Each new chemical is produced in increasing concentrations

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• I. C. Cellular Basis of Hormonal Action• 2. Second Messenger – Cyclic AMP

– d. varied end results of the different protein kinases: • Increased protein synthesis• Increased protein secretions• Change in membrane permeability, etc.• Decrease in activity

– e. above effect is terminated as cyclic AMP is destroyed by Phosphodiesterase

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Copyright © 2010 Pearson Education, Inc. Figure 16.2

Hormone (1st messenger)binds receptor.

Receptoractivates Gprotein (GS).

G proteinactivatesadenylatecyclase.

cAMP acti-vates proteinkinases.

Adenylatecyclaseconverts ATPto cAMP (2ndmessenger).

Receptor

G protein (GS)

Adenylate cyclase

Triggers responses oftarget cell (activatesenzymes, stimulatescellular secretion,opens ion channel,etc.)

Hormones thatact via cAMPmechanisms:EpinephrineACTHFSHLH

Inactiveprotein kinase

Extracellular fluid

Cytoplasm

Activeproteinkinase

GDP

GlucagonPTHTSHCalcitonin

1

2 3 4

5

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Copyright © 2010 Pearson Education, Inc. Figure 16.2, step 1


Receptor


Extracellular fluid

Cytoplasm


1

16




Receptor

G protein (GS)


Extracellular fluid

Cytoplasm

GDP


1

2

17





Receptor

G protein (GS)

Adenylate cyclase


Extracellular fluid

Cytoplasm

GDP


1

2 3

18






Receptor

G protein (GS)

Adenylate cyclase


Extracellular fluid

Cytoplasm

GDP


1

2 3 4

19





cAMP acti-vates proteinkinases.


Receptor

G protein (GS)

Adenylate cyclase

Triggers responses oftarget cell (activatesenzymes, stimulatescellular secretion,opens ion channel,etc.)


Inactiveprotein kinase

Extracellular fluid

Cytoplasm

Activeproteinkinase

GDP


1

2 3 4

5

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• I. C. Cellular Basis of Hormonal Action– 3. Second Messenger – Calcium

• a) some activated protein receptors increase intracellular calcium in the cell

• b) Extracellular hormone activates a G-protein

• c) a series of membrane bound reactions cause the release of stored calcium from the endoplasmic reticulum

• D) this calcium can– Change membrane permeability

– Change enzyme activity

– Bind to calmodulin and together, the two activate intracellular enzymes

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• I. C. Cellular Basis of Hormonal Action– 4. Hormonal effects on gene/DNA activity

• a) lipid soluble steroid hormones soluble in cell membrane

• b) bind to an intracellular receptor and both enter the nucleus

• c) the complex binds to a specific DNA receptor protein which activates a region of the DNA/chromatin

• d) transcription produces RNA which leaves the nucleus to synthesize specific proteins which are associated with the action of the hormone

23Fig. 16.3


mRNA

New protein

DNA

Hormoneresponseelements

Receptor-hormonecomplex

Receptorprotein

Cytoplasm

Nucleus

Extracellular fluid

Steroidhormone

The steroid hormonediffuses through the plasmamembrane and binds anintracellular receptor.

The receptor-hormone complex entersthe nucleus.

The receptor- hormonecomplex binds a hormoneresponse element (aspecific DNA sequence).

Binding initiatestranscription of thegene to mRNA.

The mRNA directsprotein synthesis.

Plasmamembrane

1

2

3

4

5

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Fig. 16.5

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Format of Endocrine Study

• 1. Name of gland• 2. Name and Chemistry of Hormone• 3. Normal Action of Hormone• 4. Effects of Hormone Hyposecretion • 5. Effects of Hormone Hypersecretion• 6. Mechanism of Control of Hormone Secretion

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• II. Vertebrate Hormones– A. Thyroid Gland

• 1. Anatomy - Two lobes in the region of larynx/neck, rich vascular supply, basic structure is thyroid follicle (follicle cells surrounding a central lumen or cavity which stores thyroid hormone secreted by cells) surrounded by parafollicular cells

• 2. Hormone – two similar chemicals containing amino acid thyrosine plus 3

iodines (T3) or 4 iodines (T4)

– More T4 produced but converted to (10X) potent T3 in lungs and liver

– T4 and T3 are transported in blood by thyroxine-binding globulins (TBGs)

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Fig. 45.7

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Fig. 16.8

29Copyright © 2010 Pearson Education, Inc. Figure 16.9

To peripheral tissues

T3

T3

T3

T4

T4

Lysosome

Tyrosines (part of thyroglobulinmolecule)

T4

DIT (T2)Iodine

MIT (T1)

Thyro-globulincolloid

Iodide (I–)

RoughER

Capillary

Colloid

Colloid inlumen offollicle

Thyroid follicle cells

Iodinated tyrosines arelinked together to form T3and T4.

Iodideis oxidizedto iodine.

Thyroglobulin colloid isendocytosed and combinedwith a lysosome.

Lysosomal enzymes cleaveT4 and T3 from thyroglobulincolloid and hormones diffuseinto bloodstream.

Iodide (I–) is trapped(actively transported in).

Thyroglobulin is synthesized anddischarged into the follicle lumen.

Iodine is attached to tyrosinein colloid, forming DIT and MIT.

Golgiapparatus

1

2

3

4

5

6

7

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• 3. Normal Action of Thyroid Hormones– a) regulation of metabolism and energy utilization by

tending to INCREASING metabolic rate and raising body temperature

– b) stimulates sodium-potassium pump– c) regulates / stimulates tissue growth and

development, particularly in children and particularly with the nervous and reproductive systems

• 4. Goiter = enlarged thyroid gland– a) overstimulation of gland or due to cancerous growth

of thyroid– b) understimulation of gland causes hypertrophy of

organ and gland increases in size (compensation)

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• 5. Hypothyroidism - undersecretion of gland– a) infant - cretinism, mental and physical and sexual

retardation– b) adult - myxedema, atrophy of gland (wasting

away/decrease in size), mental and physical sluggishness, overweight, slow heart rate and low body temperature

– c) treatment = ?

• 6. Hyperthyroidism - oversecretion (excessive stimulation or tumor)– a) adult - Grave’s disease

• Underweight, fast HR, nervous energy, eyes bulge due to fluid accumulation

– b) treatment = ?

• 7. Control - see Anterior Pituitary

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Fig. 16.10

Goiter Grave’s Disease

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• 8. Additional Thyroid Hormone - Calcitonin– a) normal action is to lower blood calcium and

phosphate levels by:• 1. Inhibit osteoclast activity

• 2. Accelerate bone uptake of calcium and PO4

• 3. Inhibit parathyroid hormone (see below)

– b) administration to normal individual causes hypocalcemia

– c) administration to someone with hypercalcemia causes blood calcium to return to normal levels

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• B. Parathyroid Glands• 1. Anatomy - 4

nodules attached to posterior thyroid gland– Chief cells secrete

hormone (PTH)

– Oxyphil cells - ??

• 2. Normal function of Parathyroid Hormone (PTH)

Fig. 16.11

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• 2. Normal Function of PTH– a) increases blood calcium and decreases blood

phosphate– b) stimulates absorption of both from the

gastrointestinal tract– c) stimulates osteoclasts numbers and activity – d) reabsorbs calcium from the urine into the blood, but

excretes phosphates• 3. Antagonistic to calcitonin and controlled by blood levels

of calcium by negative feedback• 4. Disorders of PTH levels

– a) hypoparathyroidism - calcium deficiency causes nerve depolarization and muscle tetany

– b) hyperparathyroidism - calcium excess due to bone destruction, moth-eaten appearance and fractures, osteitis cystica fibrosa with depression of nervous system (slow reflexes) and kidney stones

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• C. Pancreas gland– 1. Two independent functions, endocrine and exocrine

• a) Exocrine = digestive enzymes released into small intestine by acinar cells

• b) Endocrine = Islets of Langerhans produce hormones by cluster of cells (alpha, beta, delta)

– 2. Insulin - produced by beta cells as large inactive protein that has segment removed

• a) Decreases blood glucose = hypoglycemic

• b) increases transport of glucose into cells

• c) increases conversion of glucose into glycogen

• d) uses glucose in glycolysis

• e) decreases glycogenolysis and gluconeogenesis

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C. Pancreas (continued)

• 3. Glucagon - produced by alpha cells– a) antagonistic to insulin, hyperglycemic or

raises blood glucose levels – b) decrease transport of glucose into cells,

increase conversion of glycogen back to glucose, use fats in glycolysis

• 4. Somatostatin - produced by delta cells– a) inhibit both insulin and glucagon secretion,

shuts down the pancreas and re-establishes lower hormone levels

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Fig. 16.17

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Liver

Liver

Tissue cells

Stimulates glucose uptake by cells

StimulatesglycogenformationPancreas

Pancreas

Insulin

Bloodglucosefalls tonormalrange.

Stimulatesglycogenbreakdown

Bloodglucoserises tonormalrange.

Glucagon

Stimulus Bloodglucose level

Stimulus Bloodglucose level

GlycogenGlucose

GlycogenGlucose

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C. Pancreas (continued)• 5. Diabetes mellitus - copious, sweet urine -

Hyperglycemia– a) Type I diabetes - Insulin dependent diabetes

• Autoimmune disease where body destroys beta cells and individual takes insulin injections, usually associated with young

• Source of insulin?• Fetal cells, encapsulated cells, immune suppression

– b) Type II diabetes - Insulin dependent diabetes or non-insulin dependent diabetes

• Reduced responsiveness to insulin by target cells due to changes in insulin receptors, associated with older individuals

• Control blood sugar with exercise and diet• Non-insulin drugs available to regulate blood glucose (Oral

Hypoglycemic Agents)

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Insulin

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• 5. Diabetes (continued)– c) uncontrolled diabetes results in visual

problems, circulatory problems and increased breakdown of fats which produce ketone bodies and acidosis (fruity smell on breath)

• 6. Diabetic coma = too low insulin, high blood glucose, red, warm, confused, coma, needs insulin

• 7. Insulin shock = too high insulin, low blood sugar, pale, clammy, shock, needs sugar

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D. Adrenal Glands

• 1. Superior structures to kidneys-CT capsule surrounds gland with 2 regions» Adrenal Cortex

- 3 regions» Adrenal Medulla with blood

sinuses to drain gland

• 2. Adrenal Medulla - embryonically develops from sympathetic tissue– a) chromaffin cells surrounded by blood sinuses

post-ganglionic cells of the sympathetic system• No synapse• Chemicals released into blood system• Chromaffin cells innervated/controlled by pre-ganglionic sympathetic

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2. Adrenal Medulla (continued)

• b) Hormones of the Medulla– Produces and releases epinephrine and norepinephrine

– Mimics and prolongs the action of the sympathetic response to STRESS

• c) Neuroendocrine or Neurosecretory Cells• d) Tumor causes hypersecretion

– Pheochromocytomia - continuous response to stress high: (HR, BP, sugar, etc.)

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Copyright © 2010 Pearson Education, Inc. Figure 16.13a

• Cortex

Kidney

• Medulla

Adrenal gland

CapsuleZona

glomerulosa

Zonafasciculata

Zonareticularis

Adrenalmedulla

(a) Drawing of the histology of the adrenal cortex and a portion of the adrenal medulla

Medulla

Cortex

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Fig. 16.13

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3. Adrenal Cortex and Steroid hormones

• a) Anatomy of the Adrenal cortex– Essential for life– Zona glomerulosa(loops) - mineralocorticoids– Zona fasciculata(cords) - glucocorticoids– Zona reticularis(curved loops) - sex hormones

mainly androgens

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3. Adrenal Cortex and Steroid hormones b) Mineralocorticoids of the Zona glomerulosa

• Aldosterone - most abundant of mineralocorticoids

• Normal action = slight retention of sodium and water by kidneys tubules (and body)

• Increase in Na+ reabsorption - Increase blood Na+

• Increase in K+ excretion - Decrease in blood K+

• Increase in H+ to replace Na+ - Decrease in blood H+

• Increase in Cl- and HCO3- reabsorption - Raise blood

levels

• Water reabsorption increases - Increase blood Volume and increase blood pressure

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3. Adrenal Cortex and Steroid hormones c) Control of Aldosterone

• 1. Potassium levels - increase in K+ stimulates aldosterone of the cortex to be released - result - lower K+ blood levels– Low K+ blood levels decreases aldosterone secretion and less K+

excreted• 2. Renin - Angiotensin System

– Low Blood Volume due to• Dehydration• Low sodium• hemorrhage

– Causes drop in Blood Pressure– This stimulates Kidney Cells to release an enzyme - RENIN into

the blood

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• ANGIOTENSINOGEN• (plasma protein of liver)• Activated by renin of kidney

• ANGIOTENSIN I now in blood• Acted upon by enzyme secreted by lungs

• ANGIOTENSIN II• Stimulates adrenal cortex to release aldosterone and

increases Na+ and water retention• Causes vasoconstriction of arteries• BOTH RESULT IN INCREASE IN BLOOD

PRESSURE

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3d) Hyposecretion - see Addison’s Disease below

• 3e) Hypersecretion - – Aldosteronism - high sodium, low potassium

• High Blood pressure (treatable)

• Excessive water retention

• Potassium may cause problem with nerve depolarization and cause paralysis

– How can you treat this disorder?

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4. Adrenal Cortex and Glucocorticoids of Zona Fasciculata

• a) Glucocorticoids - include cortisol and cortisone and hydrocortisone (95%)

• b) Normal action = increase protein breakdown in muscle which then results in new glucose production in liver (gluconeogenesis) = hyperglycemic agents– Also release fat tissue– Improve reaction to stress by increasing glucose for

energy and improves vasoconstriction for higher BP– Anti-inflammatory - inhibit reactions involving

inflammation (decrease mast cells, stabilize lysosomes, decrease blood vessel permeability)

– Slow wound healing

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4. Glucocorticoids (continued)

• c) At higher concentrations these steroids continue to be anti-inflammatory agents (reduce inflammation and pain) – Mechanism of action - inhibiting prostaglandin

synthesis– Infrequent injections because of long action of

steroid - enter nucleus / change RNA synthesis– Injury “feels” better but takes forever to heal

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• d) Hyposecretion = Addison’s Disease– Increase in both glucocorticoids and

aldosterone– Mental and physical lethargy– Increase K+ and Decrease Na+ blood levels– Lower BP - (possible CV disorders with heart)– Increases skin pigmnetation due to increased

pituitary ACTH

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• e) Hypersecretion = Cushing’s Syndrome– Mainly glucocorticoid problem– Redistribute fat - “Moon face” and “buffalo

hump” on back (page 629) – Poor wound healing– Hyperglycemia– Hypertension and edema

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5. Adrenal Cortex and Sex Hormones of Zona Reticularis

• a) gonadocorticoids = weak androgens or male hormones– Secreted in both male and female– Low concentration causes no real contribution in

comparison to gonadal sex hormones– May be converted to more potent male and female

hormones in the peripheral tissues– May contribute to the onset of puberty

• b) Hypersecretion = Androgenital Syndrome– Obscured in adult male– prepubescent males = precocious puberty– prepubescent females = beard and enlargement of clitoris

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E. Pituitary Gland (Hypophysis)

• 1. Structure - 2 separate lobes– Anterior lobe - Adenohypophysis

• Gland which migrated from roof of mouth• Histologically, several classes of endocrine cells

– Posterior lobe - Neurohypophysis• Neural tissue migrated from base of brain• Cell bodies in hypothalamus• Nerve ending in posterior lobe with neurotransmitter

released into blood capillaries• NEUROENDOCRINE /NEUROSECRETORY

Cells

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1

2

3

4

Hypothalamicneuronssynthesize oxytocin and ADH.

Oxytocin and ADH aretransported along the hypothalamic-hypophyseal tract to the posterior pituitary.

Oxytocin and ADH arestored in axon terminals in the posterior pituitary.

Oxytocin and ADH are released into the blood when hypothalamic neurons fire.

Paraventricularnucleus Supraopticnucleus Optic chiasma

Hypothalamus

Inferiorhypophyseal artery

OxytocinADH

Infundibulum (connecting stalk)Hypothalamic-hypophysealtract

Axon terminalsPosteriorlobe ofpituitary

(a) Relationship between the posterior pituitary and the hypothalamus

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Copyright © 2010 Pearson Education, Inc. Figure 16.5b

1

2

3

When appropriatelystimulated, hypothalamic neurons secrete releasing and inhibiting hormones into the primary capillary plexus.

Hypothalamic hormones travel through the portal veins to the anterior pituitary where they stimulate or inhibit release of hormones from the anterior pituitary.

Anterior pituitaryhormones are secreted into the secondary capillary plexus.

Hypothalamus

Hypothalamic neuroncell bodies

Hypophysealportal system

Superiorhypophyseal artery

(b) Relationship between the anterior pituitary and the hypothalamus

Anterior lobeof pituitaryTSH, FSH, LH, ACTH, GH, PRL

• Primary capillary plexus• Hypophyseal portal veins• Secondary capillary plexus

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2. Hormones of the Neurohypophysis

• a) Neuroendocrine cell bodies in hypothalamus and axons in pituitary stalk and terminal branch in posterior lobe with drainage capillaries

• b) Oxytocin - peptide

– Stimulated smooth muscle of the uterus during birth

– Stimulates smooth muscle surrounding mammary glands causing milk to move into ducts for “let-down”

reflex of nursing

– Example of positive feedback

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2. Hormones of the Neurohypophysis(continued)

• c) Antidiuretic Hormone (ADH) - peptide– Causes kidneys to RETAIN water– Important to combat dehydration– Alcohol blocks the release of ADH = excess

water loss hence frequent urination while drinking and dry mouth during hangover

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3. Hormones of the Adenohypophysis

• a) Growth Hormone - protein– Normal Action - stimulates growth directly or via growth factors

(somatomedins) for a wide range of tissues during maturation and maintains tissue in adult

– Promotes protein synthesis, glycogen breakdown and hyperglycemic effects

– Hypersecretion of GH• Youngster - Gigantism - stimulates all tissue to grow early and

excessively (Andre The Giant)• Adult - Acromegaly - after normal maturation, in later years

hypersecretion causes excessive growth of soft tissue of extremities, chin, nose

– Hyposecretion of GH = pituitary dwarf

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• b) Prolactin - protein - stimulates milk PRODUCTION by mammary glands• c) Other 4 major hormones are TROPIC hormones = each

stimulates another gland to secrete its hormone into the body

– ACTH - adrenocorticotropic hormone stimulates the adrenal cortex to release glucocorticoids (cortisol)

– TSH - thyroid stimulating hormone stimulates the thyroid to secrete thyroxin

– FSH - follicle stimulating hormone stimulates egg and sperm production and estrogen release in female

– LH - luteinizing hormone promotes ovulation and release of testosterone(m) and progesterone(f)

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F. Hormones of the Hypothalamus

• 1. Neurohypophysis - oxytocin and ADH synthsized in the hypothalamic neurosecretory cell bodies, but released via the posterior lobe into capillaries (see Fig. 16.5a)

• 2. Portal System has 2 capillary beds in series or one after the other • artery capillaryvein 2nd capillary vein all over body • Pituitary Portal System has 1st capillary in hypothalamus and vein

travels down pituitary stalk to 2nd capillary bed in ANTERIOR pituitary gland

• 1st capillary picks up hypothalamic releasing hormones (RH) from other neuroendocrine cell bodies in hypothalamus

• These RH travel directly to anterior pituitary and stimulate specific anterior pituitary hormones to be released into the blood (Fig.16.5b)

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1

2

3

4

Hypothalamicneuronssynthesize oxytocin and ADH.

Oxytocin and ADH aretransported along the hypothalamic-hypophyseal tract to the posterior pituitary.

Oxytocin and ADH arestored in axon terminals in the posterior pituitary.

Oxytocin and ADH are released into the blood when hypothalamic neurons fire.

Paraventricularnucleus Supraopticnucleus Optic chiasma

Hypothalamus

Inferiorhypophyseal artery

OxytocinADH

Infundibulum (connecting stalk)Hypothalamic-hypophysealtract

Axon terminalsPosteriorlobe ofpituitary

(a) Relationship between the posterior pituitary and the hypothalamus

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Copyright © 2010 Pearson Education, Inc. Figure 16.5b

1

2

3

When appropriatelystimulated, hypothalamic neurons secrete releasing and inhibiting hormones into the primary capillary plexus.

Hypothalamic hormones travel through the portal veins to the anterior pituitary where they stimulate or inhibit release of hormones from the anterior pituitary.

Anterior pituitaryhormones are secreted into the secondary capillary plexus.

Hypothalamus

Hypothalamic neuroncell bodies

Hypophysealportal system

Superiorhypophyseal artery

(b) Relationship between the anterior pituitary and the hypothalamus

Anterior lobeof pituitaryTSH, FSH, LH, ACTH, GH, PRL

• Primary capillary plexus• Hypophyseal portal veins• Secondary capillary plexus

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Hypothalamus

Anterior pituitary

Thyroid gland

Thyroidhormones

TSH

TRH

Target cellsStimulates

Inhibits

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F. Hormones of the Hypothalamus (continued)

• 3. Each anterior pituitary hormone has its own hypothalamic RH– ACTH controlled by ACTH-RH– TSH controlled by TSH-RH – GH controlled by GH-RH (and GH-IH)– Prolactin controlled by Pro-RH (and Pro-IH)– FSH and LH controlled by same Gn-RH (gonadotropic

releasing hormone)– Therefore - if specific RH released - that stimulates

specific hormone of the anterior lobe - which stimulates another gland or body function

74

Summary

• If TH levels low, then its absence stimulates TSH-RH to be released from the hypothalamus, this RH travels directly to the anterior pituitary and specifically stimulates pituitary TSH which is released and travels all over the body, but stimulates the receptors of the thyroid gland to release and raise TH levels

• TH levels in blood now high - feedback to the hypothalamus to inhibit release of TSH-RH via negative feedback - low TSH-RH means the anterior pituitary NOT being stimulated to release TSH - no or low TSH means the thyroid is NOT being stimulated and TH levels fall again.

• Cycle continues - repeat above