Human

Anatomy and Physiology

II

Urinary System
Suggested Readings
McKinley Text
Chapter 24 – Urinary System
• Sections 24.3 – 24.8 – Urinary Physiology
• Chapter 25 – Fluid and Electrolytes
• All sections

Tortora Text
Chapter 26 – Urinary System
• Sections 26.3 – 26.10 – Urinary Physiology
Chapter 27 – Fluid and Electrolytes
• All sections
Kidneys
Functions include:
Excretion of wastes
H2O balance
• Plasma volume
Blood pressure control
• Renin
Acid-base balance
Blood Cell production
• erythropoietin
Vitamin D activation
 Urinary System

Consists of
Kidneys
Blood supply
• 20% of total flow
Transport vessels
• Ureters
• Urinary bladder
• Urethra
THE URINARY SYSTEM

Nephrons

Cortex

Medulla

Kidney
Renal pelvis

Ureter Ureter

Urinary
bladder
Urethra Capsule
(c) The kidney, in cross section.

(a) The urinary system

Kidney
Renal Calyces
Renal Cortex
outer
Renal Medulla
Inner
Renal Pelvis
Nephron
Functional unit of kidney
~ 1million / kidney
Two types
Cortical
• Shorter
• ~85%
Juxtamedullary
• Longer
• ~15%
• Osmotic gradient
Nephrons
Tubule
Blood supply
Nephron
Vascular component
Renal Artery
Afferent Arteriole
Glomerulus
• Ball-like tuft of capillaries
Efferent Arteriole
Peritubular capillaries
Renal vein
10
Efferent arteriole
Peritubular Peritubular
capillaries capillaries
Juxtaglomerular
apparatus Glomerulus

Afferent
arteriole

Glomerulus Vasa recta

(capillaries)

Collecting
duct

Loop of
Henle

(g) One nephron has two arterioles (h) Juxtamedullary nephron

and two sets of capillaries. with vasa recta
Figure 19-1g–h
 Bowman’s
Tubule capsule
Proximal tubule Distal tubule

Bowman’s capsule
Proximal tubule Descending Ascending
limb of loop limb of loop

Loop of Henle begins ends

Collecting
Ascending duct

descending
Distal tubule Descending Ascending
limb limb
Collecting duct
(j) Parts of a nephron Loop of
Henle

To bladder
Basic Renal Processes

Glomerular filtration
Fluid into tubule
Tubular reabsorption
From tubule into blood
Tubular secretion
From blood into tubule

Urine results from these three

processes.
Sites of Action
Reabsorption and
Filtration Secretion
Bowman’s capsule Proximal tubule
Distal tubule
• Hormone controlled
Collecting ducts
Peritubular capillaries Distal tubule

Loop of Henle Efferent

arteriole
Glomerulus
Creates osmotic
Afferent
gradient arteriole
Bowman’sProximal
capsule tubule
• reabsorption
KEY
= Filtration: blood to lumen Loop Collecting To renal
of duct vein
= Reabsorption: lumen to blood
Henle
= Secretion: blood to lumen
= Excretion: lumen to external To bladder and
environment external environment
Substance Fates
Substance can be
Filtered and secreted
• Some only secreted
Filtered and reabsorbed
Filtered and partially reabsorbed
Kidney Functions
Glomerular filtration
All but RBC’s and proteins
• Too big
Reabsorption
Na+, Cl-, Ca2+, PO4, water, glucose
Secretion
K+, H+, large organics
Glomerulus
Tuft of capillaries
Fenestrated
• More permeable
Surrounded by
Bowman’s capsule
Glomerular Filtration
Across three layers of the
glomerular membrane
Glomerular capillary wall
Basement membrane
• Acellular gelatinous layer
⬧ collagen and glycoproteins
Inner layer of Bowman’s capsule
• Consists of podocytes that encircle the
glomerulus tuft
Layers of Glomerulus Membrane
Glomerular Filtration
~160-180 L / day (~125 mL/min)
Moves electrolytes, water, glucose into tubules
RBC’s and most proteins are too large to be filtered
Filtration membrane
Capillary • Basement membrane
Urine • Foot processes of podocyte

<1% of filtrate
Filtration slit
Slit diaphragm
Plasma
Pore Foot processes
of podocyte

Figure 25.9c
Kidney Function

Table 19-1
 The Filtration Fraction
4 >99% of plasma
entering kidney
Efferent arteriole Peritubular returns to systemic
capillaries circulation.

5 <1% of
80%
2 20% of volume is
3 >19% of fluid
volume is reabsorbed. excreted to
Afferent filters. external
arteriole environment.
Bowman’s Remainder
1 Plasma volume capsule of nephron
entering afferent
Glomerulus
arteriole = 100%

Figure 19-4
 Podocytes
Can change shape
Control filtration

Renal failure
Large slits
Allows proteins and RBC’s in
Forces Involved in Glomerular
Filtration
Three main physical
forces involved
Glomerular capillary
blood pressure
Plasma-colloid
osmotic pressure
Bowman’s capsule
hydrostatic pressure
• (Bowman’s capsule
osmotic pressure)
Forces in Glomerular Filtration
Favours filtration
Glomerular blood Efferent
arteriole 15 mm Hg Pfluid

pressure 30 mm Hg  Net filtration

pressure =
10 mm Hg
PH 55 mm Hg

Opposes Filtration Afferent

arteriole Glomerulus
Bowman’s
capsule

Plasma-colloid PH –  – Pfluid = net filtration pressure

osmotic pressure 55 – 30 – 15 = 10mm Hg

Bowman’s capsule KEY

hydrostatic pressure
PH = Hydrostatic pressure (blood pressure)
 = Colloid osmotic pressure gradient
due to proteins in plasma but not
in Bowman’s capsule
Pfluid = Fluid pressure created by fluid in
Bowman’s capsule

Net filtration of 10
Glomerular Filtration Rate (GFR)
Depends on
Net filtration pressure
How much glomerular surface area is available
for penetration
How permeable the glomerular membrane is
• Podocytes
• Slit size can change with
infection
 Glomerular Filtration Rate (GFR)

GFR will change if the blood hydrostatic

pressure changes

Auto- Regulated
Tubuloglomerular feedback
• Local (paracrine) control
Hormones / Autonomic
• Change arteriole resistance
Tubuloglomerular Feedback
Glomerulus Distal tubule
1
GFR increases.
Efferent arteriole

2 Flow through tubule increases.

Bowman’s capsule

3 Flow past macula densa increases. 4

Macula densa 1
5
Granular cells
4 Paracrine from macula Afferent arteriole
densa to afferent arteriole 2
3

Proximal
5 Afferent arteriole constricts. tubule

Resistance in afferent
arteriole increases.
Collecting
duct

Hydrostatic pressure
in glomerulus decreases.

Loop
of
GFR decreases. Henle

Figure 19-10
Arterioles help control GFR
Resistance changes in renal arterioles alter
renal blood flow

A lower GFR if
Afferent arteriole constricts
A higher GFR if
Afferent arteriole dilates
Arterioles help control GFR
Lower GFR if
Afferent arteriole
constricts OR efferent
arteriole dilates

Higher GFR if
Afferent arteriole
dilates OR efferent
arteriole constricts
Extrinsic Control on GFR

Sympathetic control
long-term regulation
of arterial BP
Input to afferent
arterioles
• Baroreceptor reflex

Lower blood pressure

means lower GFR and
retention of fluids
Glomerular Filtration Rate (GFR)
Other examples of when GFR can change:
Plasma-colloid osmotic pressure changes
• Eg.Severely burned patient ↑ GFR
⬧ Loss of proteins from blood to repair sites lowers osmotic pressure
• Dehydrating diarrhea ↓ GFR
⬧ Loss of fluids increases osmotic pressure
 Glomerular Filtration Rate (GFR)
Other examples of when GFR can change:

Bowman’s capsule hydrostatic pressure changes

• Obstructions such as kidney stone or enlarged prostate
• elevates capsular hydrostatic pressure
• Decreases GFR
Measuring GFR

Use inulin to measure GFR

No reabsorption or
secretion

So Excretion = filtration
Movement
Trans-cellular transport
Active or passive
• Eg. Na+, glucose

Paracellular transport
Passive only
Diffusion of water, ions
Tubular Reabsorption
Passive reabsorption
No energy is required
Down electrochemical or osmotic gradients
Active reabsorption
Requires energy
Moves against electrochemical gradient
Na + Reabsorption
Tubule area % of Na+ Role of Na+
Active process reabsorbed reabsorption
Proximal 67% Plays role in
tubule reabsorbing
glucose, amino
Na+ - K+ ATPase pump acids, H2O, Cl-,
in basolateral membrane and urea
Ascending 25% Plays critical role
is essential for Na+ limb of the in kidneys’ ability
loop of Henle to produce urine
reabsorption of varying
concentrations
Distal and 8% Variable and
Affects reabsorption of collecting
tubules
subject to
hormonal
other substances control; plays
role in regulating
ECF volume
Sodium Reabsorption
Na+/K+ pump creates Na+ gradients across
membranes
Facilitates Na+ reabsorption
Reabsorption of other substances
Following the reabsorption of Na+:
Water reabsorption
• Via osmotic gradient created
Cl- reabsorption
• Via electrical gradient

Glucose – by carriers
Glucose Reabsorption
Sodium-linked glucose reabsorption in the
proximal tubule

Filtrate is similar to
interstitial fluid.

1 Na+ moving down its electrochemical gradient

Glucose and Na++ using the SGLT protein pulls glucose into the
[Na+] high [Na+] low reabsorbed cell against its concentration gradient.
[glu] low [glu] high 2
[glu] low 2 Glucose diffuses out the basolateral side of
glu glu the cell using the GLUT protein.
1
Na+ Na+
3 3 Na+ is pumped out by Na+-K+-ATPase.
[Na+] high
ATP
K+
KEY
ATP = Active transporter
= SGLT secondary active transporter
Tubule lumen Proximal tubule cell Interstitial fluid = GLUT facilitated diffusion carrier
Figure 19-13
Reabsorption of Glucose
Tubular maximum
Point where all the glucose carriers are full
excess glucose stays in the tubules and is lost in the
urine Transport maximum (T ) is transport
Transport rate of substrate (mg/min)

m
rate at saturation.

Saturation occurs.

Renal threshold is
plasma concentration
at which saturation
occurs.

Plasma [substrate] (mg/mL)

Glucose Carriers
Renal threshold
Blood glucose
level where the
carriers are full
and glucose is
seen in the urine

Eg. Diabetes
Mellitus
Urea
Reabsorption
Urea
Small, diffusible

Passive process
To equilibrium
50%
Reabsorption
Na+ (99.9%) Glucose (100%)
Na+/K+ ATPase pump Carrier-mediated
Cl- (99%) Urea (50%)
Electrical gradient Passive
Water (99%) K+ (80-90%)
Osmotic gradient secreted and reabsorbed
Aldosterone
Controls Na+/K+ ATPase pumps
Released if blood volume is low

High Aldosterone
↑ speed of pump
↑ Na+ reabsorption
↑ water reabsorption
• Decreased urine

Eg. Dehydration
 Sodium Balance

P cell of distal nephron Interstitial Blood

fluid
1 Aldosterone combines with
a cytoplasmic receptor.

Lumen
of distal 2 Hormone-receptor complex
tubule 2 1 Aldosterone initiates transcription in
the nucleus.
3 Translation and Aldosterone
protein synthesis receptor
3 New protein channels and
New pumps are made.
channels New pumps ATP
4
Proteins modulate 4 Aldosterone-induced
existing channels and pumps proteins modify existing
K+ secreted
K+ proteins.
5 K+
ATP K+
Na+ reabsorbed Na+
Na+ 5 Result is increased Na+
reabsorption and
K+ secretion.

Na+

Figure 20-12
 Renin-Angiotensin-Aldosterone
System
Regulates Na+
and blood
pressure/volume
Atrial Natriuretic Peptide (ANP)
Antagonist to Aldosterone
inactivates Na+/K+ pump
Inhibits Na+ reabsorption
Secreted by atria with
↑ BP
↑ Na+
↑ Stretch of atria (↑ volume)
 Secretion
Transfer of molecules from extracellular
fluid into tubule
Active process
K+
Na+/K+ pump
Later reabsorbed
H+
Acid-base balance
Large Organics
biotransformed
Collecting Ducts
Site of water reabsorption
Controlled by ADH
Concentrates the urine

Requires osmotic gradient

Loop of Henle
Creating a zone of high solute concentration in
renal medulla by
selective reabsorption of salt and urea

53
 Counter-Current Mechanism

Descending loop of Henle

Permeable to water
Impermeable to salts
Filtrate becomes more
concentrated
Ascending loop of Henle
Permeable to salts
• Actively reabsorbed NaCl
Impermeable to water
Filtrate becomes less concentrated
Loop of Henle: countercurrent multiplication

55
Loop of Henle: countercurrent multiplication

56
Vasa Recta
Vessel following loop of Henle
Similar Osmotic gradient in blood supply

57
Urea Recycling
Loop of Henle
Creates a large, vertical osmotic
gradient in medulla
From 100 to 1200 mosm/litre
Water reabsorption
ADH causes insertion of water pores into
the apical membrane
Water
Reabsorption
ADH
Anti-diuretic hormone
Controls permeability of
collecting ducts
Released if blood osmolarity
high

Low ADH
Impermeable to water
Dilute urine
• High volumes
Eg. Water loading
Figure 20-5b
Water Reabsorption
High ADH
Due to high blood
osmolarity
makes collecting duct
permeable to water

Concentrates urine
• Lower volume

Eg. Dehydration
Figure 20-5a
Dehydration
↑ADH
↑Aldosterone
↓ ANP

↑ water reabsorption
↓ urine
• More concentrated
Behavioral Mechanisms
Drinking replaces fluid loss
Low sodium stimulates salt appetite
Avoidance behaviors help prevent
dehydration
Desert animals avoid the heat
Water Loading
↓ADH
↓Aldosterone
↑ANP

↓ Water reabsorption
↑ urine volume
• More dilute
Proximal Tubule
67% of Na, Cl, and water reabsorption
100% glucose and amino acids are reabsorbed
K is secreted / reabsorbed (small amt)
Variable H secretion occurs
Organic ion secretion (not controlled)
Phosphate and electrolytes
controlled, variable reabsorption
Urea reabsorption
to equilibrium 50%
Distal Tubule
Variable Na reabsorption
controlled by aldosterone and ANP
Variable water reabsorption
controlled by aldosterone and ANP
Variable K secretion / reabsorption
controlled by aldosterone
Variable H secretion
depends on acid-base balance
Collecting Ducts
Variable water reabsorption
controlled by ADH
Variable H secretion
Variable Urea reabsorption
related to loop of Henle
Excretion
Excretion = filtration – reabsorption +
secretion

Clearance
Rate at which a solute disappears from the body
Non-invasive way to measure GFR
• Inulin and creatinine
Renal Clearance

RC = UV/P

RC = renal clearance rate (ml/min)

U = concentration (mg/ml) of the substance in
urine
V = flow rate of urine formation (ml/min; GFR)
P = concentration of the same substance in
plasma
Inulin Clearance
• Inulin clearance is equal to GFR

Efferent
arteriole Filtration
(100 mL/min)

Peritubular
capillaries

Glomerulus
2

Afferent
arteriole

1 Nephron
Inulin
molecules

KEY

= 100 mL of
plasma or filtrate
1 Inulin concentration 3 100 mL,
is 4/100 mL. 0% inulin
2 GFR = 100 mL /min reabsorbed

3 100 mL plasma is
reabsorbed. No inulin
is reabsorbed. 4 Inulin clearance
4 100% of inulin is 100% inulin = 100 mL/min
excreted so inulin excreted
clearance = 100 mL/min.
Figure 19-16
Glucose Clearance
Usually Zero because of 100% reabsorption
KEY
Filtration = 100 mL of
(100 mL/min) plasma or filtrate

1 Plasma concentration
2 is 4/100 mL.
2 GFR = 100 mL /min
1
Glucose 3 100 mL plasma is
molecules reabsorbed.
4 Clearance depends on
renal handling of solute.
3
100 mL,
100% glucose
reabsorbed

4 Glucose
No glucose clearance
excreted = 0 mL/min

(a) Glucose clearance

Figure 19-17a
 KEY

Excretion Filtration
(100 mL/min)
= 100 mL of
plasma or filtrate

1 Plasma concentration
2 is 4/100 mL.
2 GFR = 100 mL /min

1
3 100 mL plasma is
Urea reabsorbed.
molecules
4 Clearance depends on
renal handling of solute.
3
100 mL,
50% of urea
reabsorbed

4 Urea
50% of urea clearance
excreted = 50 mL/min

(b) Urea clearance

Figure 19-17b
 KEY

Excretion Filtration
(100 mL/min)
= 100 mL of
plasma or filtrate

1 Plasma concentration
2 is 4/100 mL.
Some 2 GFR = 100 mL /min
additional
1
Penicillin penicillin 3 100 mL plasma is
molecules secreted. reabsorbed.
4 Clearance depends on
renal handling of solute.
3 100 mL,
0 penicillin
reabsorbed

More penicillin 4 Penicillin

is excreted than clearance =
was filtered. 150 mL/min

(c) Penicillin clearance

Figure 19-17c
Micturition
The urination reflex
Autonomic control of sphincters and detrusor
muscle
CNS can over-ride or initiate
 During Filling
Bladder (detrusor) muscle is relaxed
Sphincters are contracted

Higher
CNS
input
Relaxed Bladder
(filling) (smooth muscle)
state

Internal sphincter (smooth

muscle) passively contracted
Tonic
External sphincter (skeletal discharge
muscle) stays contracted
(a) Bladder at rest
During Micturition
Stretch receptors increase their firing
Sphincters relax
Detrusor muscle contracts
Urine flows out of bladder

Stretch Higher CNS

Sensory neuron input may
receptors
facilitate or
inhibit reflex
1 Parasympathetic 1 Stretch receptors fire.
neuron
2

3 2 Parasympathetic neurons fire.

Motor neurons stop firing.

Motor neuron Smooth muscle contracts.

Tonic 3
Internal sphincter 2 discharge Internal sphincter passively
3 inhibited pulled open. External sphincter
External sphincter relaxes.
(b) Micturition
Renal Failure
Causes of renal failure
Acute
Infections / Toxic agents
Inappropriate immune responses
Obstruction of urine flow
An insufficient renal blood supply
Chronic
Hypertension
Diabetes
Chronic exposure to toxins / drugs
Renal Failure
Build-up of wastes to toxic levels
Vomiting, diarrhea, cellular necrosis
Loss of Calcium - Osteoporosis
Na+ and K+ imbalance
Affects nerve and muscle
Loss of proteins - Edema
Loss of RBC’s - Anemia
Low blood pressure (↓ renin)
Dizziness
Kidney Stones
Crystallization of minerals in either the
kidney, the ureters, or the bladder

Calcium
Oxalates
Veggies (spinach, beets)
Dehydration
Binge drinking
Acid-Base Balance
Normal pH of 7.38–7.42
H+ concentration is closely regulated
Abnormal pH
can alter tertiary structure of proteins
affects the nervous system
Acid-Base Balance
Hydrogen ion and pH balance in the body
Fatty acids CO2 (+ H2O)
Amino acids H+ input Lactic acid
Ketoacids

Plasma pH
7.38–7.42

Buffers:
• HCO3– in extracellular fluid
• Proteins, hemoglobin, phosphates in cells
• Phosphates, ammonia in urine

CO2 (+ H2O) H+ output H+

Figure 20-18
Acid-Base Balance
Acidosis
neurons become less
excitable and CNS
depression
Alkalosis
hyperexcitable

pH disturbances
with K+ disturbances
Acidosis
Metabolic Acidosis
Metabolic organic acid production
• Lactic acid (exercise)
• Ketoacids
⬧ Diabetes
Diarrhea
Organic acids intake
• Diet

Respiratory Acidosis
Production of CO2
• Acid production
Alkalosis
Metabolic Alkalosis
Vomitting
Dietary sources of bases
• Eg. Tums
Pyloric stenosis

Respiratory Alkalosis
Hyperventilation
• (high altitude)
pH Homeostasis
Buffers
Combines with or releases H+

Ventilation
75% of disturbances

Renal regulation
Slowest of the three mechanisms
Directly excreting or reabsorbing H+
Buffers
Fastest response (within seconds)
Combines with H+ so it doesn’t affect pH
Phosphate
Protein - Hemoglobin
Bicarbonate
Respiratory Compensations
pH is adjusted by changing rate and depth
of breathing
Response within minutes
CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3-
Respiratory Corrections
Plasma H+ Plasma
( pH) by Law of Mass Action PCO2

Reflex
pathway for Carotid and aortic
chemoreceptors
Central
chemoreceptors

respiratory
Respiratory

compensation control centers

Negative feedback

Negative feedback
in the
medulla

of metabolic Action potentials in somatic

acidosis motor neurons

Muscles of ventilation
Increased
breathing Rate and depth of breathing

Plasma H+ Plasma
by Law of Mass Action PCO2
( pH)

Figure 20-19
Renal Compensation: Kidney
Slowest response (within hours)
Can retain or eliminate H+ or HCO3-
Apical Na+-H+ exchanger (NHE)
Na+-HCO3– symport
Glomerulus

Bowman’s Interstitial Peritubular

capsule fluid capillary

H+-ATPase Filtration

Proximal tubule cell

HCO3– Na+

H+-K+-ATPase
Na+-NH4+ antiport 1 Na+
Secreted H+
4
Na+
H+

Na+ Na+
–
Filtered HCO3 + H+ HCO3 –
HCO3– 5
2 CA
H2O + CO2 3 CO2 + H2O CA H+ + HCO3–
Reabsorbed

6 Glutamine

7
Secreted H+ and NH4+ NH4+ KG HCO3– HCO3– 8
will be excreted Na+ Na+ Na+
Body’s Correction for Acidosis
To raise body pH
Buffers bind to H+
Breathing increases
• Decreases CO2 and H+ (via Carbonic Acid)
Kidney excrete H+ and keep Bicarbonate
Intercalated
Cells
Type A
intercalated
cells function in
acidosis
Secrete H+
Reabsorb
bicarb

Figure 20-22a
Body’s Correction for Alkalosis
To lower pH,
Buffers release H+
Breathing slows down
• Retains CO2 and H+
Kidney retains H+ and secretes Bicarbonate
 Intercalated
Cells
Type B
intercalated
cells function in
alkalosis
Secrete bicarb
Reabsorb H+

Figure 20-22b