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Final Exam Review
Summer 2010
Chapters 16, 25, and 26
Kidney Functions
• Removal of toxins, metabolic wastes, and
excess ions from the blood
• Regulation of blood volume, chemical
composition, and pH
Kidney Functions
• Gluconeogenesis during prolonged fasting
• Endocrine functions
– Renin: regulation of blood pressure and kidney
function
– Erythropoietin: regulation of RBC production
• Activation of vitamin D
Urine Movement
1. glomerulus
2. proximal convoluted tubule
3. loop of Henle
4. distal convoluted tubule
5. collecting duct
6. minor calyx
7. major calyx
8. pelvis
9. ureter
10. bladder urethra
Figure 25.5
Nephron
• Functional unit of kidney
• Units of nephron
– Renal corpuscle
• Bowman’s (glomerular) capsule
• Glomerulus
– Tubules
•
•
•
•
PCT
Loop of Henle
DCT
Collecting duct
Renal
hilum
Renal cortex
Renal medulla
Major calyx
Papilla of
pyramid
Renal pelvis
Minor calyx
Ureter
Renal pyramid
in renal medulla
Renal column
Fibrous capsule
(a) Photograph of right kidney, frontal section
(b) Diagrammatic view
Figure 25.3
Filtration Membrane
•
•
Porous membrane between the blood and the capsular
space
Consists of
1. Fenestrated endothelium of the glomerular capillaries
2. Visceral membrane of the glomerular capsule (podocytes
with foot processes and filtration slits)
3. Gel-like basement membrane (fused basal laminae of the
two other layers)
Efferent
arteriole
Glomerular capsular space
Proximal
convoluted
tubule
Afferent
arteriole
Glomerular capillary
covered by podocytecontaining visceral
layer of glomerular
capsule
Cytoplasmic extensions
of podocytes
Filtration slits
Parietal layer
of glomerular
capsule
(a) Glomerular capillaries
and the visceral layer of
the glomerular capsule
Podocyte
cell body
Fenestrations
(pores)
Glomerular capillary
endothelium (podocyte
covering and basement
membrane removed)
Foot processes
of podocyte
Figure 25.9a
Basement
membrane
Podocyte
Fenestrated
endothelium
of the glomerulus
Glomerular capsule: visceral layer
Figure 25.5
Filtration Membrane
• Allows passage of water and solutes smaller
than most plasma proteins
– Fenestrations prevent filtration of blood cells
– Negatively charged basement membrane repels
large anions such as plasma proteins
– Slit diaphragms also help to repel
macromolecules
Capillary
Filtration membrane
• Capillary endothelium
• Basement membrane
• Foot processes of podocyte
of glomerular capsule
Filtration slit
Plasma
Fenestration
(pore)
Slit diaphragm
Filtrate in
capsular
space
Foot processes
of podocyte
(c) Three parts of the filtration membrane
Figure 25.9c
Kidney Physiology: Mechanisms of
Urine Formation
• Filtrate
– Blood plasma minus proteins
• Urine
– <1% of total filtrate
– Contains metabolic wastes and unneeded
substances
Juxtaglomerular Apparatus (JGA)
• One per nephron
• Important in regulation of filtrate formation
and blood pressure
• Involves modified portions of the
– Distal portion of the ascending limb of the loop of
Henle
– Afferent (sometimes efferent) arteriole
Juxtaglomerular Apparatus (JGA)
• Granular cells (juxtaglomerular, or JG cells)
– Enlarged, smooth muscle cells of arteriole
– Secretory granules contain renin
– Act as mechanoreceptors that sense blood
pressure
– decrease in BP stimulates renin secretion
– Renin activates angiotensinogen then converted
to angiotensin II
– Angiotensin II stimulates aldosterone secretion
and vasoconstriction
Juxtaglomerular Apparatus (JGA)
• Macula densa
– Tall, closely packed cells of the ascending limb
– Act as chemoreceptors that sense NaCl content
of filtrate
SYSTEMIC BLOOD PRESSURE
(–)
Blood pressure in
afferent arterioles; GFR
Baroreceptors in
blood vessels of
systemic circulation
Granular cells of
juxtaglomerular
apparatus of kidney
GFR
Release
Stretch of smooth
muscle in walls of
afferent arterioles
Filtrate flow and
NaCl in ascending
limb of Henle’s loop
(+)
(+)
(+)
Renin
Sympathetic
nervous system
Catalyzes cascade
Targets resulting in conversion
Vasodilation of
afferent arterioles
Angiotensinogen
(+)
Macula densa cells
of JG apparatus
of kidney
Angiotensin II
(+)
Adrenal cortex
Systemic arterioles
(+)
Releases
Aldosterone
Release of vasoactive
chemical inhibited
Vasoconstriction;
peripheral resistance
Targets
Kidney tubules
Vasodilation of
afferent arterioles
Na+ reabsorption;
water follows
GFR
(+) Stimulates
(–) Inhibits
Increase
Decrease
Blood volume
Systemic
blood pressure
Myogenic mechanism
of autoregulation
Tubuloglomerular
mechanism of
autoregulation
Intrinsic mechanisms directly regulate GFR despite
moderate changes in blood pressure (between 80
and 180 mm Hg mean arterial pressure).
Hormonal (renin-angiotensin)
mechanism
Neural controls
Extrinsic mechanisms indirectly regulate GFR
by maintaining systemic blood pressure, which
drives filtration in the kidneys.
Figure 25.12
Mechanisms of Urine Formation
1. Glomerular filtration
2. Tubular reabsorption
– Returns all glucose and amino acids, 99% of
water, salt, and other components to the blood
3. Tubular secretion
– Reverse of reabsorption: selective addition to
urine
Glomerular Filtration
• Passive mechanical process driven by hydrostatic
pressure
• The glomerulus is a very efficient filter because
– Its filtration membrane is very permeable and it has a large
surface area
– Glomerular blood pressure is higher (55 mm Hg) than
other capillaries
• Molecules >5 nm are not filtered (e.g., plasma proteins)
and function to maintain colloid osmotic pressure of the
blood
Sodium Reabsorption
• Na+ (most abundant cation in filtrate)
– Primary active transport out of the tubule cell by
– Na+-K+ ATPase
Sodium Reabsorption
• Low hydrostatic pressure and high osmotic
pressure in the peritubular capillaries
• Promotes bulk flow of water and solutes
(including Na+)
Reabsorption of Nutrients, Water, and
Ions
• Na+ reabsorption provides the energy and the
means for reabsorbing most other substances
• Organic nutrients are reabsorbed by
secondary active transport
Reabsorption of Nutrients, Water, and
Ions
• Water is reabsorbed by osmosis (obligatory
water reabsorption)
• Cations and fat-soluble substances follow by
diffusion
Formation of Dilute Urine
• Filtrate is diluted in the ascending loop of
Henle
• In the absence of ADH, dilute filtrate
continues into the renal pelvis as dilute urine
• Alcohol inhibits secretion of ADH
• Na+ and other ions may be selectively
removed in the DCT and collecting duct,
decreasing osmolality to as low as 50 mOsm
Formation of Concentrated Urine
• Depends on the medullary osmotic gradient
and ADH
• ADH triggers reabsorption of H2O in the
collecting ducts
• Facultative water reabsorption occurs in the
presence of ADH so that 99% of H2O in filtrate
is reabsorbed
Regulation of Water Output: Influence
of ADH
• Water reabsorption in collecting ducts is
proportional to ADH release
•  ADH  dilute urine and  volume of body
fluids
•  ADH  concentrated urine
Tubular Secretion
• Reabsorption in reverse
– K+, H+, NH4+, creatinine, and organic acids move
from peritubular capillaries or tubule cells into
filtrate
• Disposes of substances that are bound to
plasma proteins
Tubular Secretion
• Eliminates undesirable substances that have
been passively reabsorbed (e.g., urea and uric
acid)
• Rids the body of excess K+
• Controls blood pH by altering amounts of H+
or HCO3– in urine
Regulation of Water Output: Influence
of ADH
• Hypothalamic osmoreceptors trigger or inhibit
ADH release
• Other factors may trigger ADH release via
large changes in blood volume or pressure,
e.g., fever, sweating, vomiting, or diarrhea;
blood loss; and traumatic burns
Osmolality
Na+ concentration
in plasma
Plasma volume
BP (10–15%)
Stimulates
Osmoreceptors
in hypothalamus
Negative
feedback
inhibits
Stimulates
Inhibits
Baroreceptors
in atrium and
large vessels
Stimulates
Posterior pituitary
Releases
ADH
Antidiuretic
hormone (ADH)
Targets
Collecting ducts
of kidneys
Effects
Water reabsorption
Results in
Osmolality
Plasma volume
Scant urine
Figure 26.6
Disorders of Water Balance: Hypotonic
Hydration
• Cellular over hydration or water intoxication
• Occurs with renal insufficiency or rapid
excess water ingestion or SIADH
• ECF is diluted  hyponatremia  net
osmosis into tissue cells  swelling of cells 
severe metabolic disturbances (nausea,
vomiting, muscular cramping, cerebral edema)
 possible death
Homeostatic Imbalances of ADH
• ADH deficiency — diabetes insipidus; huge
output of urine and intense thirst
• ADH hypersecretion (after neurosurgery,
trauma, or secreted by cancer cells)—
syndrome of inappropriate ADH secretion
(SIADH)
Disorders of Water Balance: Edema
• Atypical accumulation of IF fluid  tissue swelling
• Due to anything that increases flow of fluid out of
the blood or hinders its return
•  Blood pressure
•  Capillary permeability (usually due to inflammatory
chemicals)
• Incompetent venous valves, localized blood vessel
blockage
• Congestive heart failure, hypertension,  blood
volume
• Loss or decrease production of plasma proteins, liver
disease, urine loss of proteins
Edema
• Hindered fluid return occurs with an
imbalance in colloid osmotic pressures, e.g.,
hypoproteinemia ( plasma proteins)
– Fluids fail to return at the venous ends of capillary
beds
– Results from protein malnutrition, liver disease, or
glomerulonephritis
Edema
• Blocked (or surgically removed) lymph vessels
– Cause leaked proteins to accumulate in IF
–  Colloid osmotic pressure of IF draws fluid from
the blood
– Results in low blood pressure and severely
impaired circulation
Composition of Body Fluids
• Electrolytes
– Dissociate into ions in water; e.g., inorganic salts,
all acids and bases, and some proteins
– The most abundant (most numerous) solutes
– Have greater osmotic power than nonelectrolytes,
so may contribute to fluid shifts
– Determine the chemical and physical reactions of
fluids
Composition of Body Fluids
• Water: the universal solvent
• Solutes: nonelectrolytes and electrolytes
– Nonelectrolytes: most are organic
• Do not dissociate in water: e.g., glucose, lipids,
creatinine, and urea
Extracellular and Intracellular
Fluids
• Each fluid compartment has a distinctive
pattern of electrolytes
• ECF
– All similar, except higher protein content of
plasma
• Major cation: Na+
• Major anion: Cl–
Extracellular and Intracellular
Fluids
• ICF:
– Low Na+ and Cl–
– Major cation: K+
– Major anion HPO42–
Central Role of Sodium
• Most abundant cation in the ECF
• The body’s water volume is closely tied to the
level of sodium in its respective space
• Sodium salts in the ECF contribute 280 mOsm of
the total 300 mOsm ECF solute concentration
• Na+ leaks into cells and is pumped out against its
electrochemical gradient
• Na+ content may change but ECF Na+
concentration remains stable due to osmosis
Fluid Movement Among
Compartments
• Regulated by osmotic and hydrostatic
pressures
• Water moves freely by osmosis; osmolalities
of all body fluids are almost always equal
• Two-way osmotic flow is substantial
• Ion fluxes require active transport or channels
• Change in solute concentration of any
compartment leads to net water flow
Electrolyte Balance
• Importance of salts
– Controlling fluid movements
– Excitability
– Secretory activity
– Membrane permeability
Regulation of Sodium Balance:
Aldosterone
• Na+ reabsorption
– 65% is reabsorbed in the proximal tubules
– 25% is reclaimed in the loops of Henle
• Aldosterone  active reabsorption of
remaining Na+
• Water follows Na+ if ADH is present
Regulation of Sodium Balance:
Aldosterone
• Renin-angiotensin mechanism is the main
trigger for aldosterone release
– Granular cells of JGA secrete renin in response to
• Sympathetic nervous system stimulation
•  Filtrate osmolality
•  Stretch (due to  blood pressure)
Regulation of Sodium Balance:
Aldosterone
• Renin catalyzes the production of angiotensin
II, which prompts aldosterone release from
the adrenal cortex
• Aldosterone release is also triggered by
elevated K+ levels in the ECF
• Aldosterone brings about its effects slowly
(hours to days)
K+ (or Na+) concentration
in blood plasma*
Renin-angiotensin
mechanism
Stimulates
Adrenal cortex
Negative
feedback
inhibits
Releases
Aldosterone
Targets
Kidney tubules
Effects
Na+ reabsorption
K+ secretion
Restores
Homeostatic plasma
levels of Na+ and K+
Figure 26.8
Regulation of Potassium Balance
• Influence of aldosterone
– Stimulates K+ secretion (and Na+ reabsorption) by
principal cells
– Increased K+ in the adrenal cortex causes
• Release of aldosterone
• Potassium secretion
Regulation of Sodium Balance: ANP
• Released by atrial cells in response to stretch
( blood pressure)
• Effects
• Decreases blood pressure and blood volume:
–  ADH, renin and aldosterone production
–  Excretion of Na+ and water
– Promotes vasodilation directly and also by
decreasing production of angiotensin II
Stretch of atria
of heart due to BP
Releases
Negative
feedback
Atrial natriuretic peptide (ANP)
Targets
Hypothalamus
and posterior
pituitary
JG apparatus
of the kidney
Effects
Adrenal cortex
Effects
Renin release*
ADH release
Angiotensin II
Aldosterone release
Inhibits
Inhibits
Collecting ducts
of kidneys
Vasodilation
Effects
Na+ and H2O reabsorption
Results in
Blood volume
Results in
Blood pressure
Figure 26.9
Acid-Base Balance
• pH affects all functional proteins and
biochemical reactions
• Normal pH of body fluids
– Arterial blood: pH 7.4
– Venous blood and IF fluid: pH 7.35
– ICF: pH 7.0
• Alkalosis or alkalemia: arterial blood pH >7.45
• Acidosis or acidemia: arterial pH < 7.35
Acid-Base Balance
• Most H+ is produced by metabolism
– Phosphoric acid from breakdown of phosphoruscontaining proteins in ECF
– Lactic acid from anaerobic respiration of glucose
– Fatty acids and ketone bodies (strong organic
acids) or from fat metabolism
– H+ liberated when CO2 is converted to HCO3– in
blood
Acid-Base Balance
• Concentration of hydrogen ions is regulated
sequentially by
– Chemical buffer systems: rapid; first line of
defense
– Brain stem respiratory centers: act within 1–3 min
– Renal mechanisms: most potent, but require
hours to days to effect pH changes
Chemical Buffer Systems
•
Chemical buffer: system of one or more
compounds that act to resist pH changes
when strong acid or base is added
1. Bicarbonate buffer system
2. Phosphate buffer system
3. Protein buffer system
Bicarbonate Buffer System
• Mixture of H2CO3 (weak acid) and salts of
HCO3– (e.g., NaHCO3, a weak base)
• Buffers ICF and ECF
• The only important ECF buffer
Bicarbonate Buffer System
• If strong acid is added:
– HCO3– ties up H+ and forms H2CO3
• HCl + NaHCO3  H2CO3 + NaCl
– pH decreases only slightly, unless all available
HCO3– (alkaline reserve) is used up
– HCO3– concentration is closely regulated by the
kidneys
Bicarbonate Buffer System
• If strong base is added
– It causes H2CO3 to dissociate and donate H+
– H+ ties up the base (e.g. OH–)
• NaOH + H2CO3  NaHCO3 + H2O
– pH rises only slightly
– H2CO3 supply is almost limitless (from CO2
released by respiration) and is subject to
respiratory controls
Physiological Buffer Systems
• Respiratory and renal systems
– Act more slowly than chemical buffer systems
– Have more capacity than chemical buffer systems
Respiratory Regulation of H+
• Respiratory system eliminates CO2
• A reversible equilibrium exists in the blood:
– CO2 + H2O  H2CO3  H+ + HCO3–
• During CO2 unloading the reaction shifts to
the left (and H+ is incorporated into H2O)
• During CO2 loading the reaction shifts to the
right (and H+ is buffered by proteins)
Respiratory Regulation of H+
• Hypercapnia activates medullary
chemoreceptors
• Rising plasma H+ activates peripheral
chemoreceptors
– More CO2 is removed from the blood
– H+ concentration is reduced
Respiratory Regulation of H+
• Alkalosis depresses the respiratory center
– Respiratory rate and depth decrease
– H+ concentration increases
• Respiratory system impairment causes acidbase imbalances
– Hypoventilation  respiratory acidosis
– Hyperventilation  respiratory alkalosis
Acid-Base Balance
• Chemical buffers cannot eliminate excess
acids or bases from the body
– Lungs eliminate volatile carbonic acid by
eliminating CO2
– Kidneys eliminate other fixed metabolic acids
(phosphoric, uric, lactic acids and ketones) and
prevent metabolic acidosis
Renal Mechanisms of Acid-Base
Balance
• Most important renal mechanisms
– Conserving (reabsorbing) or generating new HCO3–
– Excreting HCO3–
• Generating or reabsorbing one HCO3– is the
same as losing one H+
• Excreting one HCO3– is the same as gaining
one H+
Renal Mechanisms of Acid-Base
Balance
• Renal regulation of acid-base balance depends
on secretion of H+
• H+ secretion occurs in the PCT and in
collecting duct type A intercalated cells:
– The H+ comes from H2CO3 produced in reactions
catalyzed by carbonic anhydrase inside the cells
Reabsorption of Bicarbonate
• Tubule cell luminal membranes are impermeable to
HCO3–
–
–
–
–
CO2 combines with water in PCT cells, forming H2CO3
H2CO3 dissociates
H+ is secreted, and HCO3– is reabsorbed into capillary blood
Secreted H+ unites with HCO3– to form H2CO3 in filtrate,
which generates CO2 and H2O
• HCO3– disappears from filtrate at the same rate that it
enters the peritubular capillary blood
Generating New Bicarbonate Ions
• Two mechanisms in PCT and type A
intercalated cells
– Generate new HCO3– to be added to the alkaline
reserve
• Both involve renal excretion of acid via
secretion and excretion of H+ or NH4+
Excretion of Buffered H+
• Dietary H+ must be balanced by generating
new HCO3–
• Most filtered HCO3– is used up before filtrate
reaches the collecting duct
Excretion of Buffered H+
• Intercalated cells actively secrete H+ into
urine, which is buffered by phosphates and
excreted
• Generated “new” HCO3– moves into the
interstitial space via a cotransport system and
then moves passively into peritubular capillary
blood
Abnormalities of Acid-Base Balance
• Respiratory acidosis and alkalosis
• Metabolic acidosis and alkalosis
Respiratory Acidosis and Alkalosis
• The most important indicator of adequacy of
respiratory function is PCO2 level (normally 35–45 mm
Hg)
– PCO2 above 45 mm Hg  respiratory acidosis
• Most common cause of acid-base imbalances
• Due to decrease in ventilation or gas exchange
• Characterized by falling blood pH and rising PCO2
Respiratory Acidosis and Alkalosis
• PCO2 below 35 mm Hg  respiratory alkalosis
– A common result of hyperventilation due to stress
or pain
Metabolic Acidosis and Alkalosis
• Any pH imbalance not caused by abnormal
blood CO2 levels
• Indicated by abnormal HCO3– levels
Metabolic Acidosis and Alkalosis
• Causes of metabolic acidosis
– Ingestion of too much alcohol ( acetic acid)
– Excessive loss of HCO3– (e.g., persistent diarrhea)
– Accumulation of lactic acid, shock, ketosis in
diabetic crisis, starvation, and kidney failure
Metabolic Acidosis and Alkalosis
• Metabolic alkalosis is much less common than
metabolic acidosis
– Indicated by rising blood pH and HCO3–
– Caused by vomiting of the acid contents of the
stomach or by intake of excess base (e.g.,
antacids)
Respiratory and Renal
Compensations
• If acid-base imbalance is due to malfunction
of a physiological buffer system, the other one
compensates
– Respiratory system attempts to correct metabolic
acid-base imbalances
– Kidneys attempt to correct respiratory acid-base
imbalances
Respiratory Compensation
• In metabolic acidosis
– High H+ levels stimulate the respiratory centers
– Rate and depth of breathing are elevated
– Blood pH is below 7.35 and HCO3– level is low
– As CO2 is eliminated by the respiratory system,
PCO2 falls below normal
Respiratory Compensation
• Respiratory compensation for metabolic
alkalosis is revealed by:
– Slow, shallow breathing, allowing CO2
accumulation in the blood
– High pH (over 7.45) and elevated HCO3– levels
Renal Compensation
• Hypoventilation causes elevated PCO2
• (respiratory acidosis)
– Renal compensation is indicated by high HCO3–
levels
• Respiratory alkalosis exhibits low PCO2 and high
pH
– Renal compensation is indicated by decreasing
HCO3– levels
Mechanisms of Hormone Action
• Hormone action on target cells
1. Alter plasma membrane permeability of
membrane potential by opening or closing ion
channels
2. Stimulate synthesis of proteins or regulatory
molecules
3. Activate or deactivate enzyme systems
4. Induce secretory activity
5. Stimulate mitosis
Mechanisms of Hormone Action
•
Two mechanisms, depending on their chemical nature
1. Water-soluble hormones (all amino acid–based hormones
except thyroid hormone)
• Cannot enter the target cells
• Act on plasma membrane receptors
• Coupled by G proteins to intracellular second
messengers that mediate the target cell’s response
Mechanisms of Hormone Action
2. Lipid-soluble hormones (steroid and thyroid
hormones)
•
Act on intracellular receptors that directly activate
genes
Target Cell Specificity
• Target cells must have specific receptors to
which the hormone binds
– ACTH receptors are only found on certain cells of
the adrenal cortex
– Thyroxin receptors are found on nearly all cells of
the body
Target Cell Activation
• Target cell activation depends on three factors
1. Blood levels of the hormone
2. Relative number of receptors on or in the target
cell
3. Affinity of binding between receptor and
hormone
The Posterior Pituitary
• Contains axons of hypothalamic neurons
• Stores antidiuretic hormone (ADH) and
oxytocin
• ADH and oxytocin are released in response to
nerve impulses
• Both use PIP-calcium second-messenger
mechanism at their targets
Oxytocin
• Stimulates uterine contractions during
childbirth by mobilizing Ca2+ through a PIP2Ca2+ second-messenger system
• Also triggers milk ejection (“letdown” reflex)
in women producing milk
• Plays a role in sexual arousal and orgasm in
males and females
Antidiuretic Hormone (ADH)
• Hypothalamic osmoreceptors respond to
changes in the solute concentration of the
blood
• If solute concentration is high
– Osmoreceptors depolarize and transmit impulses
to hypothalamic neurons
– ADH is synthesized and released, inhibiting urine
formation
Antidiuretic Hormone (ADH)
• If solute concentration is low
– ADH is not released, allowing water loss
• Alcohol inhibits ADH release and causes
copious urine output
Growth Hormone (GH)
• Produced by somatotrophs
• Stimulates most cells, but targets bone and
skeletal muscle
• Promotes protein synthesis and encourages
use of fats for fuel
• Most effects are mediated indirectly by
insulin-like growth factors (IGFs)
Adrenocorticotropic Hormone
(Corticotropin)
• Regulation of ACTH release
– Triggered by hypothalamic corticotropin-releasing
hormone (CRH) in a daily rhythm
– Internal and external factors such as fever,
hypoglycemia, and stressors can alter the release
of CRH
Glucocorticoids (Cortisol)
• Cortisol is the most significant glucocorticoid
– Released in response to ACTH, patterns of eating
and activity, and stress
– Prime metabolic effect is gluconeogenesis—
formation of glucose from fats and proteins
– Promotes rises in blood glucose, fatty acids, and
amino acids
Mineralocorticoids
• Regulate electrolytes (primarily Na+ and K+) in
ECF
– Importance of Na+: affects ECF volume, blood
volume, blood pressure, levels of other ions
– Importance of K+: sets RMP of cells
• Aldosterone is the most potent
mineralocorticoid
– Stimulates Na+ reabsorption and water retention
by the kidneys
Mechanisms of Aldosterone
Secretion
1. Renin-angiotensin mechanism: decreased blood
pressure stimulates kidneys to release renin, triggers
formation of angiotensin II, a potent stimulator of
aldosterone release
2. Plasma concentration of K+: Increased K+ directly
influences the zona glomerulosa cells to release
aldosterone
3. ACTH: causes small increases of aldosterone during
stress
4. Atrial natriuretic peptide (ANP): blocks renin and
aldosterone secretion, to decrease blood pressure
Adrenal Medulla
• Chromaffin cells secrete epinephrine (80%)
and norepinephrine (20%)
• These hormones cause
– Blood glucose levels to rise
– Blood vessels to constrict
– The heart to beat faster
– Blood to be diverted to the brain, heart, and
skeletal muscle
Adrenal Medulla
• Epinephrine stimulates metabolic activities,
bronchial dilation, and blood flow to skeletal
muscles and the heart
• Norepinephrine influences peripheral
vasoconstriction and blood pressure
Short-term stress
More prolonged stress
Stress
Nerve impulses
Hypothalamus
CRH (corticotropinreleasing hormone)
Spinal cord
Corticotroph cells
of anterior pituitary
To target in blood
Preganglionic
sympathetic
fibers
Adrenal medulla
(secretes amino acidbased hormones)
Catecholamines
(epinephrine and
norepinephrine)
Short-term stress response
1. Increased heart rate
2. Increased blood pressure
3. Liver converts glycogen to glucose and releases
glucose to blood
4. Dilation of bronchioles
5. Changes in blood flow patterns leading to decreased
digestive system activity and reduced urine output
6. Increased metabolic rate
Adrenal cortex
(secretes steroid
hormones)
ACTH
Mineralocorticoids
Glucocorticoids
Long-term stress response
1. Retention of sodium
and water by kidneys
2. Increased blood volume
and blood pressure
1. Proteins and fats converted
to glucose or broken down
for energy
2. Increased blood glucose
3. Suppression of immune
system
Figure 16.16
Parathyroid Hormone
• PTH—most important hormone in Ca2+
homeostasis
• Functions
– Stimulates osteoclasts to digest bone matrix
– Enhances reabsorption of Ca2+ and secretion of
phosphate by the kidneys
– Promotes activation of vitamin D (by the kidneys);
increases absorption of Ca2+ by intestinal mucosa
• Negative feedback control: rising Ca2+ in the
blood inhibits PTH release
Hypocalcemia (low blood Ca2+) stimulates
parathyroid glands to release PTH.
Rising Ca2+ in
blood inhibits
PTH release.
Bone
1 PTH activates
osteoclasts: Ca2+
and PO43S released
into blood.
Kidney
2 PTH increases
2+
Ca reabsorption
in kidney
tubules.
3 PTH promotes
kidney’s activation of vitamin D,
which increases Ca2+ absorption
from food.
Intestine
Ca2+ ions
PTH Molecules
Bloodstream
Figure 16.12
Glucagon
• Major target is the liver, where it promotes
– Glycogenolysis—breakdown of glycogen to
glucose
– Gluconeogenesis—synthesis of glucose from lactic
acid and noncarbohydrates
– Release of glucose to the blood
Insulin
• Effects of insulin
– Lowers blood glucose levels
– Enhances membrane transport of glucose into fat
and muscle cells
– Participates in neuronal development and learning
and memory
– Inhibits glycogenolysis and gluconeogenesis
Homeostatic Imbalances of Insulin
• Diabetes mellitus (DM)
– Due to hyposecretion or hypoactivity of insulin
– Three cardinal signs of DM
• Polyuria—huge urine output
• Polydipsia—excessive thirst
• Polyphagia—excessive hunger and food consumption
• Hyperinsulinism:
– Excessive insulin secretion; results in hypoglycemia,
disorientation, unconsciousness
Table 16.4
Gonadotropins
• Follicle-stimulating hormone (FSH) and
luteinizing hormone (LH)
• Secreted by gonadotrophs of the anterior
pituitary
• FSH stimulates gamete (egg or sperm)
production
• LH promotes production of gonadal hormones
• Absent from the blood in prepubertal boys
and girls
Homeostatic Imbalances of Growth
Hormone
• Hypersecretion
– In children results in gigantism
– In adults results in acromegaly
• Hyposecretion
– In children results in pituitary dwarfism
Homeostatic Imbalances of
Glucocorticoids
• Hypersecretion—Cushing’s syndrome
–
–
–
–
Depresses cartilage and bone formation
Inhibits inflammation
Depresses the immune system
Promotes changes in cardiovascular, neural, and
gastrointestinal function
• Hyposecretion—Addison’s disease
– Also involves deficits in mineralocorticoids
• Decrease in glucose and Na+ levels
• Weight loss, severe dehydration, and hypotension
Homeostatic Imbalances of TH
• Hyposecretion in adults—myxedema; endemic
goiter if due to lack of iodine
• Hyposecretion in infants—cretinism
• Hypersecretion—Graves’ disease