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Hormone Receptors
- Protein/glycoprotein
- Located in cell membrane or within cytoplasm, nucleus, or mitochondrion
- Target = cell with specific receptors/hormones
- No recpetor, no effect on hormone
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Hormone Effects
1. Cause synthesis of new proteins (ex. make new enzymes
2. Modify transcription/translation rate of existing proteins (make more/less)
3. Modify activity/function of existing enzymes (increase/decrease enzyme activity)
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Local vs. Circulating Hormones
- 1. Ciruclating Hormones: "endocrines = "typical hormone" (most abundant)
- *Transported in blood; affect target cells all over the body
- 2. Paracrine Hormones: act only on nearby cells (do not go through the body)
- *E.g. somatostatin from delta cells in pancreatic islets inhibits secretion of insulin by beta cells
- 3. Autocrine Hormones: Act on cell that secretes it
- *E.g. Helper T cells release interleukin 2 which stimulates the proliferation of cell that secretes it
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Amino Acid Derivatives (biogenic amines)
- A. Derivatives of tyrosine
- *Catecholamines (Epi and Norepi)
- *Thyroid Hormones (T3 and T4 thyroxine)
- B. Derivative of tryptophan
- *Melatonin from pineal
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Peptide (and protein) Hormones
- Usually produced as prohormones
- Prohormone = enzyme = active hormone
- A. All hypothalamic hormones (releasing hormones, and ADH and OT)
- B. All anterior pituitary hormones
- C. All pancreatic hormones
- D. Calcium-regulating hormones (PTH, Calcitonin)
- E. Digestive hormones
- F. Erythropoietin (kidneys)
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Lipid Derivatives
- A. Derivatives of cholesterol = steroid hormones
- *From gonads (androgens, estrogens, progestins)
- *From adrenal cortex (mineralcorticoids [aldosterone], glucocorticoids [cortisol], gonadocorticoids [androgens])
- *From kidneys (calcitrol [Vit D])
- B. Derivatives of arachadonic acid
- *Eicosanoids
- Prostoglandins (many tissues)
- Leukotrienes (white blood cells)
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Water-soluble hormone transport
- Hormone NOT bound to carrier molecule
- E.g. Catecholamines, peptides, proteins
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Lipid-soluble hormone transport
- Transport requires a carrier molecule (e.g. steroids, thyroid hormones)
- Functions of the carrier
- a. Increases solubility in plasma and ECF
- b. Decreases hormone loss at kidney
- c. Forms a hormone reserve
- Hormone reserve
- *Equilibrium exists between "bound" and "free" form
- *Free fraction usually a very small % of total
- *More of the bound form is released as free form is used up.
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Removal of Hormones from Circulation
- Bind to receptors (some inside of cells)
- Broken down by enzymes in liver, kidneys
- Broken down by enzymes in plasma or ECF
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Mechanisms of Action
- Depend upon lipid vs. water solubility
- a. Water-soluble hormone: act on membrane receptors
- b. Lipid-soluble hormone: act intracelluarly
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First and Second Messengers
- First Messenger (hormone)
- Bind to receptor (usually a G-protein)
- Second Messenger
- E.g. cAMP, cGMP, Ca2+
- Functions:
- *Enzyme activator
- *Enzyme inhibitor
- *Enzyme cofactor (facilitates function)
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Amplification
- Mechanism of action
- Many 2nd messengers of the same type are formed
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Receptor Cascade
- Mechanism of action
- Different 2nd messengers activated, sequence of biochemical reactions
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Downregulation and Upregulation
- Downregulation
- Hormone levels high
- Number of receptors and sensitivity to hormones went DOWN
- Upregulation
- Hormone levels low
- Opposite effects
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Membrane Receptors
- G Proteins and cAMP
- *Hormone binds receptor, G protein activated
- a. Activate adenylate cyclase, which will INCREASE cAMP, or...
- b. Activate PDE, which will LOWER cAMP
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Increased cAMP Levels
- cAMP (2nd messenger) activates kinases
- Kinases phosphorylate proteins which...
- *Open membrane channels and alter enzyme acitivity
- (PDE inactivates cAMP)
- E.g. Hormones
- β receptors for E and NE
- PTH and calcitonin ([Ca2+])
- FSH and LH (ovaries and testis)
- E.g. Disease = Cholera - altered G protein function
- Toxin activates G proteins
- G proteins can't be turned off
- Causes increased cAMP levels in gut
- Increased pumping of Cl- out of cells
- Na+ and water follow = diarrhea, dehydration, death
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Decreased cAMP Levels
- E.g. E and NE at α2 recpetors
- G protein activates PDE; adenylate cyclase is not activated
- *PDE breaks down cAMP to AMP causing:
- -Decrease cAMP
- -Decrease of kinase activation
- -Decrease enzyme activity
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Intracellular Receptors
- Hormone must be lipid soluble
- *Binds receptors in cytoplasm
- *Hormone receptor complex enters nucleus
- *Alters gene expression
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Cytoplasmic Receptors
- E.g. testosterone
- Binds receptor in cytoplasm
- Hormone receptor complex enters nucleus
- Alters gene expression
INTRACELLULAR HORMONE RECEPTORS
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Binding to nuclear and/or mitochondrial receptors
- E.g. thyroid hormone
- a. binds receptors on mitochondria
- *increase ATP production and use(NA/K pump)
- b. Bind receptors in nucleus
- * Alters gene expression
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Endocrine reflexes triggered by:
- 1. Humoral stimuli (concentration in CSF)
- e.g. parathyroid gland
- .↓ [CA²] in CSF → release PTH
- 2. Hormonal Stimuli (Tropic hormones)
- e.g. adrenal cortex
- . Release cortisol in respond to ACTH
- 3. Neural Stimuli (action potential)
- e.g. posterior pituitary
- . Action potentials cause ADH and OT release
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