Chapter 26

The Urinary System

 Urinary system

• Organs that excrete &

eliminate urine:
– Kidneys (paired filters)
– Ureters (paired tubes)
– Urinary bladder
(muscular sac)
– Urethra (exit tube)
5 Homeostatic Functions of Urinary System
1. Regulate blood volume and blood pressure:
– by adjusting volume of water lost in urine
– releasing erythropoietin and renin
2. Regulate plasma ion concentrations:
– Na, K, and Cl ions (by controlling quantities lost in urine)
– Ca levels (through synthesis of calcitriol)
3. Help stabilize blood pH:
– by controlling loss of hydrogen ions and bicarbonate ions in
urine
4. Conserve valuable nutrients:
– by preventing excretion while excreting organic waste
products
5. Assist liver to detoxify poisons
 Typical Adult Kidney
• Is about 10 cm long, 5.5 cm wide, and 3 cm
thick & weighs about 150 g
• Each kidney is protected and stabilized by 3
concentric layers of connective tissue:
1. renal capsule-A layer of collagen fibers that
covers outer surface of entire organ
2. adipose capsule-A thick layer of adipose tissue
that surrounds renal capsule
3. renal fascia-A dense, fibrous outer layer that
anchors kidney to surrounding structures
 Internal anatomy
• Cortex – outer layer; contains bulk of
nephrons
• Medulla – contains ~6-18 renal pyramids
– Pyramids – consist mostly of urine collecting
tubules arranged in parallel fashion
– Renal columns (extensions of cortex) separate
pyramids…lobe = pyramid & surrounding cortex
& capsule
• Pelvis – minor calyces (4 or 5) collect urine
from pyramids & major calyces (2 or 3)
empty into ureter
Internal Anatomy
 Blood Supply
• Approximately one-
fourth (1200 ml) of
systemic cardiac
output flows through
the kidneys each
minute
• Arterial flow into
and venous flow out
of the kidneys follow
similar paths
 Renal nerve supply
• Renal plexus (off-shoot of celiac plexus)
– Mostly from least thoracic & 1st lumbar splanchnic
nerves (SNS)
– Sympathetic fibers are vasomotor to renal arterioles
to regulate renal blood flow
• Adjusts rate of urine formation:
– by changing blood flow and blood pressure at
nephron
• Stimulates release of renin:
– which restricts losses of water and salt in urine by
stimulating reabsorption at nephron
 Nephron
• Glomerulus (tuft of
capillaries) assoc w/ renal
tubule
• Bowman’s (glomerular)
capsule – the end of the
renal tubule
– Bowman’s capsule + the
enclosed glomerulus are
referred to as the renal
corpuscle
• Proximal convoluted tubule
(thin segment)
• Loop of Henle
– Thick & thin segments
• Distal convoluted tubule
(thick segment)
– Empty into collecting ducts
(in pyramids)…into minor
calyces
 Capillary beds of the nephron
• Glomerulus – produces
the filtrate
– Both fed & drained by
arterioles
– Afferent is larger
diameter than efferent..
higher pressure for
pushing fluid & solutes
out of blood
• Peritubular capillaries
– reclaim most of the
filtrate
– Low pressure & porous
for absorption from the
tubules
 Filtration membrane
• 3 layers allow passage of water
& solutes smaller than plasma
proteins
– 1.Fenestrated endothelium of the
glomerular capillaries
• Prevents passage of blood cells
but allows passage of other
plasma components
– 2.Visceral membrane of the
glomerular capsule (made of
podocytes)
– 3.The intervening basement
membrane (lamina densa) made
up of the fused basal laminas of
the other 2 layers
• Restricts passage of all but the
smallest proteins & permits most
other solutes to pass
 Juxtaglomerular apparatus
• At initial point of distal convoluted tubule
• JG cells are present in the arteriole walls & act
as mechanoreceptors to sense BP in the afferent
arteriole
– JG cells are enlarged, smooth mm cells filled
w/secretory granules filled w/renin
• Macula densa is a group of tall, packed cells in
the distal tubule & lies adjacent to the JG cells
– These are chemo/osmoreceptors that respond to
changes in solute content of the filtrate in the lumen
of the tubule
 Kidney physiology
• Account for ~1% of total body weight yet consume 20-
25% of all O2 used by the body at rest
• Process ~1880 L (47 gallons) of blood derived fluid/day
– Only ~1% of this (1.5 L) actually leaves the body as
urine
• 1000-1200 ml of blood/min pass thru glomeruli (650
ml of which is plasma)
• Equivalent to filtering your entire plasma volume
>60x/day
• Usually produce concentrated urine:
– 1200–1400 mOsm/L (4 times plasma concentration)
 Mechanisms of Urine Formation
• Urine formation
and adjustment of
blood composition
involves three
major mechanisms
1. Glomerular
filtration
2. Tubular
reabsorption
3. Secretion
 Glomerular filtration
• Mostly a passive process driven by hydrostatic P
– Glomerular filtration membrane is 1000s x more
permeable than regular capillary membranes
– Glomerular BP is higher than in other caps (55
mmHg versus <18 mmHg)
– Kidneys produce ~ 180 L filtrate/day while other
body caps produce ~3-4 L/day combined
– Usually, molecules <3 nm (water, glucose, AAs,
nitrogenous wastes) can pass…molecules >7-9 nm
are usually completely barred from entering tubule
• Plasma proteins in the caps help maintain osmotic P
• proteins./RBCs in urine usually indicates a problem w/the
filtration membrane
Glomerular Hydrostatic Pressure (GHP)

• Is blood pressure in glomerular capillaries

• Tends to push water and solute molecules:
– out of plasma & into the filtrate
• Is significantly higher than capillary pressures
in systemic circuit:
– due to arrangement of vessels at glomerulus
 Capsular Hydrostatic Pressure (CsHP)

• Opposes glomerular hydrostatic pressure

• Pushes water and solutes:
– out of filtrate & into plasma
• Results from resistance to flow along nephron
and conducting system
• Averages about 15 mm Hg
Blood Colloid Osmotic Pressure (BCOP)

• Tends to draw water out of filtrate & into plasma

• Opposes filtration
• Averages 25 mm Hg
 Glomerular filtration rate (GFR)
• The total amount of filtrate formed by the kidneys
per minute (avg. 125 ml/min)
• About 10% of fluid delivered to kidneys leaves
bloodstream & enters capsular spaces
• It is directly proportional to the net filtration
pressure
– Glomerular BP- (osmotic P of glomerular blood +
capsular hydrostatic P of other fluids in glomerulus)
– An increase in NFP (arterial BP) increases GFR & vice
versa (dehydration will increase glomerular osmotic
pressure & decrease GFR)
Glomerular Filtration Rate (GFR)
 Regulation of Glomerular Filtration

• If the GFR is too high:

– Needed substances cannot be reabsorbed quickly
enough and are lost in the urine
• If the GFR is too low:
– Everything is reabsorbed, including wastes that are
normally disposed of
 3 factors governing GFR at cap beds

• 1. Total surface area available for filtration

• 2. Filtration membrane permeability
• 3. Net filtration pressure

• The normal GFR in both kidneys in adults is

~125 ml/min (7.5 L/hour..180 L/day)
 3 controls of renal blood flow
• These all function to keep GFR at a fairly
constant level
• 1. Renal autoregulation (intrinsic)
• 2. Renin-angiotensin system (hormonal)
• 3. Neural controls (SNS)
 Intrinsic controls (autoregulation)
• Maintains GFR despite changes in local blood
pressure and blood flow by changing diameters of
afferent arterioles, efferent arterioles, and
glomerular capillaries (Myogenic mechanism)
• Reduced blood flow or glomerular blood pressure
triggers:
– dilation of afferent arteriole, dilation of glomerular
capillaries, & constriction of efferent arterioles
• Rise in renal blood pressure:
– stretches walls of afferent arterioles, causes smooth
muscle cells to contract, constricts afferent arterioles, &
decreases glomerular blood flow
Intrinsic controls (autoregulation), cont.
• Tubuloglomerular feedback mechanism –
directed by macula densa of JGA
– Cells respond to high filtrate flow rate & increased
osmotic signals that leads to a release of chemicals to
cause severe vasoconstriction of the afferent
arterioles
– When macula densa cells are exposed to slowly
flowing filtrate or filtrate w/low osmolarity they
promote vasodilation of afferent arterioles
– Macula densa cells also send signals to JG cells to set
renin-angiotensin mechanism into motion
 SNS control of GFR
• SNS (+) causes vasoconstriction of afferent
arterioles & slows filtrate production
• W/extreme stress or an emergency, the
autoregulatory mechanisms may be overcome in
order to shunt blood to vital areas like the brain,
skeletal mm, & heart at the expense of the
kidneys
– This also indirectly (+) the renin-angiotensin
mechanism by (+) the macula densa cells
– SNS can also directly (+) JG cells to release renin by
the binding of norepi
 Renin-angiotensin mechanism
• JG cells of JGA release renin…renin acts on
angiotensinogen (made in liver)..converts to angiotensin
II by ACE (angiotensin converting enzyme)
– Angiotensin II is a powerful vasoconstrictor that
causes a rise in mean arterial BP
• It’s also (+) adrenal cortex to release aldosterone…
renal tubules reclaim more Na…more water
follows…blood vol & BP rises
– There are more AT II receptors on the efferent
arteriole than the afferent…it increases the glomerular
hydrostatic pressure
 Triggers of renin release
• 1. Reduced stretch of JG cells (hemorrhage, salt
depletion, deH2O)
• 2. JG cell (+) via macula densa cells
– promotes vasodilation of afferent arterioles
while simultaneously (+) JG cells to
vasoconstrict efferent arterioles
• 3. Direct (+) of JG cells via SNS fibers due to
decline in osmotic concentration of tubular
fluid at macula densa
 Tubular reabsorption
• Our total blood volume is filtered every 45
minutes so the majority of filtrate must be
reabsorbed & returned to the blood
• Virtually all organic nutrients are reabsorbed
(glucose, AAs, etc)…kidneys function to
maintain or restore normal plasma levels
• Reabsorption of H2O and many ions is
continuously monitored & adjusted in response
to hormonal signals
• Reabsorption may be either active or passive
4 Types of Carrier-Mediated Transport

1. Facilitated diffusion
2. Active transport
3. Cotransport
4. Countertransport
5 Characteristics of Carrier-Mediated Transport

1. A specific substrate binds to carrier protein:

– facilitates movement across membrane
2. A given carrier protein usually works in 1
direction only
3. Distribution of carrier proteins varies among
portions of cell surface
4. The membrane of a single tubular cell
contains many types of carrier protein
5. Carrier proteins, like enzymes, can be
saturated
 Sodium reabsorption
• Na is the most abundant cation in the filtrate
• Occurs predominately by primary active transport
& is transcellular (transepithelial)
• 80% of total energy used for active transport is
devoted to Na
• Net effect of Na reabsorption via active transport
is to provide the energy & means for reabsorbing
most other solutes
 Passive tubular reabsorption

• Diffusion, facilitated diffusion, & osmosis all

require no E
• As Na ions move into peritubular capillary blood
it sets up an electrical gradient favoring passive
reabsorption of anions (i.e. Cl- & HCO3-)
 Obligatory water reabsorption
• Na movement establishes a strong osmotic
gradient & water is “obliged” to follow salt into
the peritubular caps
• …as water leaves the tubules it causes the [ ] of
solutes left in the filtrate to increase…setting up
a concentration gradient into the peritubular
capillaries
• Usually recovers 85% of filtrate produced
 Secondary active transport

• Examples include glucose, AAs, lactate, vitamins,

& most cations
• A common carrier moves Na down its [ ] gradient
pulling the solute with (symport)
 The Transport Maximum (Tm)

• If nutrient concentrations rise in tubular fluid:

– reabsorption rates increase until carrier proteins are
saturated
• Concentration higher than transport maximum:
– exceeds reabsorptive abilities of nephron
– some material will remain in the tubular fluid and
appear in the urine
• Determines the renal threshold
 Renal Threshold
• Is the plasma concentration at which a specific
compound or ion begins to appear in urine
• Varies with the substance involved
• Glucose- is approximately 180 mg/dl
– If plasma glucose is greater than 180 mg/dl Tm of
tubular cells is exceeded & glucose appears in urine…
glycosuria
• AA’s- lower than that of glucose (65 mg/dl)
– Amino acids commonly appear in urine after a
protein-rich meal…aminoaciduria
 Nonreabsorbed substances
• Some substances may:
– 1. Lack carriers
– 2. Be lipid insoluble
– 3. Too large to pass thru plasma membrane pores of
the tubular cells

• The most important of these substances are the nitrogenous

end products of protein & nucleic acid metabolism: urea,
creatinine, & uric acid
 Reabsorption and Secretion at the PCT

• PCT cells normally reabsorb 60–70% of filtrate

produced in renal corpuscle
• Reabsorbed materials enter peritubular fluid and
diffuse into peritubular capillaries
 Proximal convoluted tubule
• The most active section for reabsorption
• All glucose, lactate, & AAs
• 65% of Na in filtrate/~65 % of H2O
• 90% bicarb, 50% Cl, 55% K

• Of the 125 ml/min of filtered fluid into the renal

tubules, ~40 ml remains to enter the loop of
Henle
 Loop of Henle
• Epithelium permeability changes
dramatically from PCT
• For the first time, H2O reabsorption is not
coupled w/Na reabsorption
• 25%Na, 10%H2O, 35% Cl, 30% K
 Distal convoluted tubule
• Most reabsorption by this time is hormonally
regulated as the body needs
• If necessary, nearly all H2O & Na reaching this
point can be reclaimed
– Reabsorption of the remaining Na is largely
dependent on aldosterone (causes collecting ducts to
become more permeable to Na)
• w/o hormones, the DCT & collecting duct are
relatively impermeable to H2O
– Reabsorption is now dependent on ADH, which
makes the collecting ducts more permeable to H2O
 Countercurrent multiplier
• Is exchange that occurs between 2 parallel
segments of loop of Henle which are very close
together, separated only by peritubular fluid
• They have very different permeability
characteristics
– the thin, descending limb-fluid flows toward renal
pelvis
– the thick, ascending limb-fluid flows toward cortex
 Countercurrent multiplier, cont.
• 1. Filtrate entering the descending limb is isosmotic
(isotonic) to both blood plasma & surrounding cortical
interstitial fluid
• 2. As filtrate flows from the cortex into the medulla in
the descending limb water leaves the tubule by osmosis
& the relative solute content (osmolality) of the filtrate
increases from 300 to 1200 mOsm
• 3. As filtrate flows thru bend of loop & goes into the
ascending limb, tubule permeability changes from
water perm/solute imperm to the opposite (water
imperm/solute perm)
 Countercurrent multiplier, cont.
• 4. Salt leaves the ascending limb via active transport,
diluting the filtrate as it approaches the cortex
– The 2 limbs in the loop of Henle act to establish the [ ] gradient
in the medullary interstitial fluid
– The descending limb produces increasingly salty filtrate
– The ascending limb uses this high salt [ ] to maintain the high
osmolality of the interstitial fluid in the medulla
• 5. Vasa recta vessels are specialized to allow for sluggish
blood flow. The osmotic gradient is maintained b/c the
blood in the vasa recta continuously equilibrates w/ the
interstitial fluid…it becomes more [ ] as it follows the
descending loop & less [ ] as it approaches the cortical
region
Formation of dilute
urine
• Tubular filtrate is normally
dilutes as it travels up the
ascending limb
• The collecting ducts are
normally impermeable to
water so no further
reabsorption occurs
• In absence of ADH the
dilute urine keeps traveling
to the renal pelvis & out in
the urine
Formation of [ ]
urine
• ADH inhibits urine output
(diuresis) by increasing the
collecting ducts permeability to
water
• With maximal ADH secretion
99% of water in filtrate is
reabsorbed & returned to blood
• Water reabsorption that depends
on the presence of ADH is
called facultative water
reabsorption
• ~15% of filtrate volume (27
liters/day)
Formation of Dilute and Concentrated Urine
 Tubular secretion
• Essentially the reverse of tubular reabsorption
• Blood entering peritubular capillaries:
– contains undesirable substances that did not cross
filtration membrane at glomerulus
• More dominant in the PCT (& DCT/C.D.’s)
• Important for:
– 1. Disposing of substances not already in the filtrate
(i.e. certain drugs – penicillin)
– 2. Elimination of certain undesirable end-products
reabsorbed by passive processes (urea/uric acid)
– 3. Ridding the body of excessive K ions
– 4. Controlling blood pH
 Hydrogen Ions
• Are secreted by sodium-linked countertransport:
– in exchange for Na+ in tubular fluid
• Bicarbonate ions diffuse into bloodstream:
– buffer changes in plasma pH
• Hydrogen Ion Secretion
– Acidifies tubular fluid
– Elevates blood pH
– Accelerates when blood pH falls
 Acidosis
• Lactic acidosis develops after exhaustive muscle
activity
• Ketoacidosis develops in starvation or diabetes
mellitus
• Response to Acidosis
– PCT and DCT deaminate amino acids:
• ties up H+ & yields ammonium ions (NH4+)
and HCO3—
– Ammonium ions are pumped into tubular fluid
– Bicarbonate ions enter bloodstream through
peritubular fluid
 Alkalosis
• Abnormally high blood pH
• Can be caused by prolonged aldosterone
stimulation:
– which stimulates secretion
Nephrolithiasis
Extracorporeal shock wave lithotripsy
Pyelogram

Figure 26–17
 Composition of urine
• Color
– Clear to pale yellow…darker w/ [ ]
– Color may change w/diet, drugs, infection (cloudy),
etc
• Odor
– Varies w/diet, more odorous if stagnant as bacteria
metabolize the urea solutes (ammonia smell)
• pH
– Usually ~6.0…may vary b/t 4.5-8.0 w/diet
• Specific gravity
– Varies w/solute [ ]; solutes may precipitate out w/high
[]
 Chemical composition of urine
• 95% water/5% solutes
• Nitrogenous waste products:
• Urea – from normal breakdown of AAs
• Uric acid – end product of nucleic acid metabolism
• Creatinine – a metabolite of creatine phosphate
(regeneration of ATP—sk mm)
• Urea, Na, K, Ph, SO4, creatinine, uric acid
– Smaller amts of Ca, Mg, HCO3 ions
• A healthy adult produces:
– 1200 ml per day (0.6% of filtrate)
– with osmotic concentration of 800–1000 mOsm/L
General Characteristics
of Normal Urine

Table 26–5
Urine Storage & Transport
 3 Layers of the Ureter Wall
• Inner mucosa:
– transitional epithelium and lamina propria
• Middle muscular layer:
– longitudinal and circular bands of smooth muscle
• Outer connective-tissue layer:
– continuous with fibrous renal capsule and
peritoneum
• Peristaltic contractions begin at renal pelvis
sweep along ureter & force urine toward urinary
bladder approx. every 30 seconds
 Bladder physiology
• Trigone is at base where openings for 2 ureters & 1
urethra are found…infection location
• 3 layers:
– Mucosa (transitional epithelium)
– Muscular layer (detrusor mm) – inner/outer longitudinal
layers & middle circular layer of smooth mm
– Fibrous adventitia covering
• Empty bladder folds into rugae…as it fills it expands to
hold urine
– Moderately full bladder holds ~500 ml (1 pint) but it can hold
more than double that if necessary
 Micturition
• As the bladder fills with urine:
– stretch receptors in urinary bladder stimulate sensory
fibers in pelvic nerve
– stimulus travels from afferent fibers in pelvic nerves to
sacral spinal cord
– efferent fibers in pelvic nerves stimulate ganglionic
neurons in wall of bladder
– postganglionic neuron in intramural ganglion stimulates
detruscor muscle contraction
– interneuron relays sensation to thalamus
– projection fibers from thalamus deliver sensation to
cerebral cortex
– voluntary relaxation of external urethral sphincter causes
relaxation of internal urethral sphincter
 Micturition, cont.
• Afferent impulses are transmitted to the brain
w/~200ml of filling giving urge to void
• Micturition center is in the dorsolateral pons & acts as
an on/off switch, signaling the PsNS neurons that (+)
contraction of the detrusor mm & relaxation of the
internal & external urethral sphincters allowing urine to
be voided
• We can voluntarily choose not to void & micturition
reflex will occur again w/200-300 ml more
accumulation…we can keep delaying to a certain point
until we can no longer avoid the inevitable
Micturition (Voiding or Urination)