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paracrine chemical signaling
chemical released from cell and has effects on nearby target cell, local communication
autocrine chemical signaling
chemical released from cell and has effect on itself
endocrine chemical signaling
chemical produced by cell, released into bloodstream for wide spread, systemic effects
endocrine glands
ductless glands that release hormones to act on distant target cells
primary endocrine organ
primary function or organ is to produce hormones
secondary endocrine organ
has its own specialized function but also secretes hormones
classification of hormones
amines, lipid derivatives, peptide
amines
derived from tyrosine
examples: thyroid hormone, epinephrine, norepinephrine, dopamine
lipid derivatives
steroid hormones: derived from cholesterol
eicosanoids: derived from arachidonic acid
peptide hormones
majority of hormones
synthesized as prohormones
stored in secretory vescicles
prohormone
inactive protein, becomes active later when its ready to be used, made in abundance
hormones in the blood
transport: circulate in the blood either free form or bound to a carrier (hydrophobic hormones need help)
breakdown of hormones: uptake by target cell and degradation, liver and kidney, urinary excretion
bioavailability
amount of hormone available to exert action on target cell, has potential/ability to bind to its target
half life
the time it takes for concentration of hormone in blood to decrease to 50% its initial concentration
hormone receptors
proteins
reactive to one hormone or specific to a group of hormones
small concentrations of a hormone have a large effect
undergo structural changes when ligand binds
2 types
intracellular receptors
plasma membrane receptors
intracellular receptors
steroid hormones, thyroid hormones
altered gene expression
slow acting - once receptor binds, it acts as transcription factor (increases expression of gene they are responsible for binding to) which impacts gene expression
plasma membrane receptors
peptide hormones, most amines
fact acting
altered activity of proteins in cell
G protein coupled receptor (GPCR)
integral protein with 7 transmembrane spanning domains
G proteins
have 3 subunits: alpha, beta, gamma
alpha is able to bind to GTP and GDP
desensitization
decreases a cell’s response to hormone
decrease in number of receptors on plasma membrane
receptors degraded in lysosomes or proteosomes
sensitization
increases cell’s response to hormone
increase in receptor number on plasma membrane
vesicle fusion of stored receptors with membrane
phosphorylation of receptor
can lead to desensitization or sensitization
anterior pituitary
cells that release hormones into circulation
Under the control of hypothalamic hormones (hypophyseal portal system)
posterior pituatary
axon terminals of neurons whose cell body is in hypothalamus
neuroendocrine cells
Release antidiuretic hormone (ADH) and oxytocin (OXT) from posterior lobe
stores and releases hormones produced by the hypothalamus
Oxytocin
peptide hormone
maternal behaviors and love
stimulus for release:
breast - suckling of lactating breast
uterus - cervical stretch during labor (positive feedback)
detected by sensory receptors in breast and uterus
milk let down response
baby suckling, stimulates posterior, causes contraction of milk producing cells, pushes milk out
Antidiuretic Hormone (ADH) / Vasopressin
peptide hormone
purpose: kidney to reabsorb water → when we are dehydrated
stimulus for release:
increase in plasma osmolarity
detected by osmoreceptors in hypothalamus
target organ: kidney
effect: increased water reabsorption
put water into blood and then stop producing ADH
hypothalamus releases Growth Hormone Releasing Hormone (GHRH) and Growth Hormone Inhibiting Hormone (GHIH) for anterior pituitary to regulate release of
Growth Hormone
hypothalamus releases Prolactin Inhibiting Hormone (PIH) for anterior pituitary to inhibit release of
Prolactin
hypothalamus releases Thyrotropin Releasing Hormone (TRH) for anterior pituitary to release
Thyroid Stimulating Hormone
hypothalamus releases Corticotropin Releasing Hormone (CRH) for anterior pituitary to release
Adrenocorticotropic Hormone
hypothalamus releases Gonadotropin Releasing Hormone (GnRH) for anterior pituitary to release
Luteinizing hormone (LH) and Folicle Stimulating Hormone (FSH)
5 types of secretory cells
somototrophs
lactotrophs
thyrotrophs
Corticotrophs
Gonadotrophs
Somototrophs
Growth Hormone
Lactotrophs
prolactin
Thyrotrophs
thyroid stimulating hormone
Corticotrophs
adrenocorticotropic hromone
Gonadotrophs
follicle stimulating hormone (FSH) and Luteinizing Hormone (LH)
Prolactin
peptide hormone
involved in breast feeding
normally prolactin isn’t being released because of PIH
pregnancy and suckling on breast decrease PIH release and sensory receptors send afferent signal to hypothalamus
Stimulates growth and development of mammary glands; stimulate milk SYNTHESIS
what does prolactin inhibit
GnRH - FSH and LH not being produced and influence menstrual cycle - stops when not released
hypterprolactinemia
pituitary gland making too much prolactin causing menstrual cycle irregularities
Growth Hormone
Stimulus for release: has a circadian rhythm with a peak in release in early hours of sleep
effect on target organs through 2 mechanisms
binds to GH receptors on target cell directly
stimulates production of insulin like growth factors (IGFs)
more potent form of growth factor
binds to receptors on target cells indirectly
effect on target organ: stimulates cell growth and division
excess growth hormone
before puberty: gigantism
after puberty: acromegaly
less growth hormone
before puberty: dwarfism
follicle
the smallest functional unit of thyroid
fluid (colloid) filled sphere lined by simple cubodial epithelial cells (follicle cells)
synthesis of thyroid hormone
parafollicular cells - C cells
synthesis/release of calcitonin hormone
in between follicle cells
calcitonin
released when too much Ca2+ in blood
inhibit osteoclasts
increase excretion of Ca2+ by kidney
prevent absorption of Ca2+ by digestive system
thyroid hormone T4 & T3
derived from amino acid tyrosine (amine hormone)
T4: 4 iodine atoms
T3: 3 iodine atoms
T4
most abundant form of thyroid hormone
T3
body prefers this form to actually use
synthesis of thyroid hormone
iodide ions (I-) are transported from blood into follicular cell (TSH dependent)
TSH receptors on thyroid follicular cells which turns on iodide pump
iodide ions (I-) converted into iodine atoms (I) by thyroid peroxidase (called activating iodine) then paired with thyroglobulin → get pushed into the colloid
thyroglobulin makes a lot of tyrosine (imagine it being a packet of tyrosine)
In the colloid thyroid hormone is made and then brought back into the cell - thyroglobulin has T3 and T4 in it
When the body needs the hormone, it brings in chunks of colloid and and fuses with a lysosome to free T3 and T4
through diffusion, T4 and T3 enter into capillaries and bind with TBG (carrier protein to help thyroid hormone travel because it doesn’t travel well in the blood by itself)
actions of thyroid hormone
fast, strong, short increase in rate of cellular respiration → increased production of ATP
3 receptor locations within a cell
cytoplasmic receptors: storage
mitochondria receptors: increase rate of ATP production
nucleus: increase gene transcription and act like transcription factor (inc/dec certain proteins being made in the cell)
specific actions:
increased metabolic rate (heat production)
increased HR and BP
stimulate RBC formation → increase oxygen delivery
trigger bone remodeling process
hypothyroidism
thyroid hormone = increased ATP
not having enough means you’re tired
iodine deficiency
TRH → TSH → tells thyroid gland to make more thyroid hormone but it can’t because lack of iodine → can’t tell hypothalamus to stop releasing TRH
TRH and TSH levels high → causes growth of thyroid gland
hyperthyroidism
most common cause: graves disease
antibody activated TSH receptor
goiter and increased T4 & T3
body making protein abnormally → thyroid stimulating antibody
binds to TSH receptor → making lots of thyroid hormone and tells hypothalamus to stop releasing TSH but keeps on making more thyroid hormone
parathyroid gland
4 small glands on posterior surface of thyroid
collection of parathyroid principle cells
secrete parathyroid hormone (PTH) in response to low levels of Ca2+ levels in the blood
effects:
stimulates osteoclasts
increased absorption of Ca2+ by kidney
stimulates formation of calcitriol (active form of vitamin D) by kidney
adrenal glands
composed of
outer cortex: corticosteroids - makes steroid hormones
inner medulla: epinephrine and norepinephrine
layers of outer cortex: corticosteroids (outer to inner)
zona glomerulosa
zona fasciculata
zona reticularis
hormones of adrenal cortex: zona glomerulosa
mineralcorticoids (hormone class) : regulation of sodium and potassium levels in ECF
aldosterone (main type of hormone): released in response to low levels of Na+
reabsorption of Na+ from urine, seat glands, and salivary glands at the expense of K+
hormones of adrenal cortex: zona fasciculata
glucocorticoids (hormone class): regulation of carbohydrate levels in ECF, anti-inflammatory properties (reduce activity of immune systems - helps reduce pain)
cortisol (specific hormone): speed up rate of glucose synthesis and glycogen formation
helps regulate glucose and tells body to make new glucose molecules
hormones of adrenal cortex: zona reticularis
sex hormones → usually make sex hormones
weak androgens, useful as precursors for the production of estrogen and testosterone by other tissues
influence muscle mass and sex drive in adult women
hypothalamic pituitary adrenal (HPA) axis
stress or higher brain centers cause hypothalamus to release CRH → anterior pituitary releases ACTH → enters blood stream and reaches adrenal cortex (zona fasciculata) and stimulates it to release cortisol
cortisol effects on body:
↑ glucose formation (gluconeogenesis)
↑ fatty acid release
↓ protein synthesis (breaks muscle protein)
This provides energy during stress
Chronic stress
Cortisol stays high for long periods
Brain receptors become desensitized
So cortisol can’t shut off CRH properly anymore
will keep releasing CRH → ACTH → cortisol
short term stress response
stressful response kicks on cortisol → makes glucose and rebuilding glycogen reserves
long term stress response
starvation
Atrioventricular valves
tricuspid (right atria and ventricle) and bicuspid/mitral (left atria and ventricle)
Between the atria and ventricles
Semilunar valves
aortic and pulmonary
heart wall laters (outer to inner)
parietal pericardium (faces outer cavity)
epicardium
myocardium
endocardium
cardiomyocytes
cardiac muscles cells
striated (because of thick and thing filaments)
branched at ends
mono-nucleated
reduced SR system but extensive T tubule system
intercalated discs
intercalated discs
specialized, zigzag-shaped junctions connecting individual cardiac muscle cells (cardiomyocytes), crucial for synchronizing heart contractions; where cells come in contacct
desmosomes (thick proteins holding them together, adhesion proteins) - mechanical couples
gap junctions - electrical coupling