The urinary system

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Human
Anatomy
& Physiology
SEVENTH EDITION
Elaine N. Marieb
Katja Hoehn
PowerPoint® Lecture Slides
prepared by Vince Austin,
Bluegrass Technical
and Community College
CHAPTER
25The Urinary
System
P A R T A

Kidney Functions
 Filter 200 liters of blood daily, allowing toxins,
metabolic wastes, and excess ions to leave the
body in urine
 Regulate volume and chemical makeup of the
blood
 Maintain the proper balance between water and
salts, and acids and bases

Other Renal Functions
 Gluconeogenesis during prolonged fasting
 Production of rennin to help regulate blood
pressure and erythropoietin to stimulate RBC
production
 Activation of vitamin D

Other Urinary System Organs
 Urinary bladder – provides a temporary storage
reservoir for urine
 Paired ureters – transport urine from the kidneys to
the bladder
 Urethra – transports urine from the bladder out of
the body

Urinary System Organs
Figure 25.1a

Kidney Location and External Anatomy
 The kidneys lie in a retroperitoneal position in the
superior lumbar region
 The right kidney is lower than the left because it is
crowded by the liver
 The lateral surface is convex; the medial surface is
concave
 The renal hilus leads to the renal sinus
 Ureters, renal blood vessels, lymphatics, and
nerves enter and exit at the hilus

Layers of Tissue Supporting the Kidney
 Renal capsule – fibrous capsule that prevents
kidney infection
 Adipose capsule – fatty mass that cushions the
kidney and helps attach it to the body wall
 Renal fascia – outer layer of dense fibrous
connective tissue that anchors the kidney

Internal Anatomy (Frontal Section)
 Cortex – the light colored, granular superficial
region
 Medulla – exhibits cone-shaped medullary (renal)
pyramids separated by columns
 The medullary pyramid and its surrounding capsule
constitute a lobe
 Renal pelvis – flat funnel shaped tube lateral to the
hilus within the renal sinus

PLAY InterActive Physiology ®:
Anatomy Review, page 6
Internal Anatomy
 Major calyces – large branches of the renal pelvis
 Collect urine draining from papillae
 Empty urine into the pelvis
 Urine flows through the pelvis and ureters to the
bladder

Internal Anatomy
Figure 25.3b

Blood and Nerve 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
 The nerve supply is via the renal plexus
Anatomy Review, page 5

Renal Vascular Pathway
Figure 25.3c

The Nephron
 Nephrons are the structural and functional units
that form urine, consisting of:
 Glomerulus – a number of capillaries associated
with a renal tubule
 Glomerular (Bowman’s) capsule – blind, cup-
shaped end of a renal tubule that completely
surrounds the glomerulus

The Nephron
 Renal corpuscle – the glomerulus and its
Bowman’s capsule
 Glomerular endothelium – fenestrated epithelium
that allows solute-rich, virtually protein-free filtrate
to pass from the blood into the glomerular capsule
Urinary: Anatomy Review, pages 7-9

The Nephron
Figure 25.4a, b

Renal Tubule
 Proximal convoluted tubule (PCT) – composed of
cuboidal cells with numerous microvilli and
mitochondria
 Reabsorbs water and solutes from filtrate and
secretes substances into it

Renal Tubule
 Loop of Henle – a hairpin-shaped loop of the renal
tubule
 Proximal part is similar to the proximal convoluted
tubule
 Proximal part is followed by the thin segment
(simple squamous cells) and the thick segment
(cuboidal to columnar cells)
 Distal convoluted tubule (DCT) – cuboidal cells
without microvilli that function more in secretion
than reabsorption

Renal Tubule
Figure 25.4b

Connecting Tubules
 The distal portion of the distal convoluted tubule
nearer to the collecting ducts

Connecting Tubules
 Two important cell types are found here
 Intercalated cells
 Cuboidal cells with microvilli
 Function in maintaining the acid-base balance of
the body
 Principal cells
 Cuboidal cells without microvilli
 Help maintain the body’s water and salt balance
Anatomy Review, pages 12–15, 17–19

Nephrons
 Cortical nephrons – 85% of nephrons; located in
the cortex
 Juxtamedullary nephrons:
 Are located at the cortex-medulla junction
 Have loops of Henle that deeply invade the
medulla
 Have extensive thin segments
 Are involved in the production of concentrated
urine

Nephron Anatomy
Figure 25.5a

Capillary Beds of the Nephron
 Every nephron has two capillary beds
 Glomerulus
 Peritubular capillaries
 Each glomerulus is:
 Fed by an afferent arteriole
 Drained by an efferent arteriole

Capillary Beds of the Nephron
 Blood pressure in the glomerulus is high because:
 Arterioles are high-resistance vessels
 Afferent arterioles have larger diameters than
efferent arterioles
 Fluids and solutes are forced out of the blood
throughout the entire length of the glomerulus

Capillary Beds
 Peritubular beds are low-pressure, porous
capillaries adapted for absorption that:
 Arise from efferent arterioles
 Cling to adjacent renal tubules
 Empty into the renal venous system
 Vasa recta – long, straight efferent arterioles of
juxtamedullary nephrons

Capillary Beds
Figure 25.5a

Vascular Resistance in Microcirculation
 Afferent and efferent arterioles offer high
resistance to blood flow
 Blood pressure declines from 95mm Hg in renal
arteries to 8 mm Hg in renal veins

Vascular Resistance in Microcirculation
 Resistance in afferent arterioles:
 Protects glomeruli from fluctuations in systemic
blood pressure
 Resistance in efferent arterioles:
 Reinforces high glomerular pressure
 Reduces hydrostatic pressure in peritubular
capillaries

Juxtaglomerular Apparatus (JGA)
 Where the distal tubule lies against the afferent
(sometimes efferent) arteriole
 Arteriole walls have juxtaglomerular (JG) cells
 Enlarged, smooth muscle cells
 Have secretory granules containing renin
 Act as mechanoreceptors

 Macula densa
 Tall, closely packed distal tubule cells
 Lie adjacent to JG cells
 Function as chemoreceptors or osmoreceptors
 Mesanglial cells:
 Have phagocytic and contractile properties
 Influence capillary filtration

Figure 25.6

Filtration Membrane
 Filter that lies between the blood and the interior of
the glomerular capsule
 It is composed of three layers
 Fenestrated endothelium of the glomerular
capillaries
 Visceral membrane of the glomerular capsule
(podocytes)
 Basement membrane composed of fused basal
laminae of the other layers

Filtration Membrane
Figure 25.7a

Filtration Membrane
PLAY InterActive Physiology ®: Anatomy Review, page 11
Figure 25.7c

Mechanisms of Urine Formation
 The kidneys filter the body’s entire plasma volume
60 times each day
 The filtrate:
 Contains all plasma components except protein
 Loses water, nutrients, and essential ions to
become urine
 The urine contains metabolic wastes and unneeded
substances

Mechanisms of Urine Formation
 Urine formation
and adjustment of
blood composition
involves three
major processes
 Glomerular
filtration
 Tubular
reabsorption
 Secretion
Figure 25.8

Glomerular Filtration
 Principles of fluid dynamics that account for tissue
fluid in all capillary beds apply to the glomerulus
as well
 The glomerulus is more efficient than other
capillary beds because:
 Its filtration membrane is more permeable
 Glomerular blood pressure is higher
 It has a higher net filtration pressure
 Plasma proteins are not filtered and are used to
maintain oncotic pressure of the blood

Net Filtration Pressure (NFP)
 The pressure responsible for filtrate formation
 NFP equals the glomerular hydrostatic pressure
(HPg) minus the oncotic pressure of glomerular
blood (OPg) combined with the capsular
hydrostatic pressure (HPc)
NFP = HPg – (OPg + HPc)

Glomerular Filtration Rate (GFR)
 The total amount of filtrate formed per minute by
the kidneys
 Factors governing filtration rate at the capillary
bed are:
 Total surface area available for filtration
 Filtration membrane permeability
 Net filtration pressure

 GFR is directly proportional to the NFP
 Changes in GFR normally result from changes in
glomerular blood pressure

Figure 25.9

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

Regulation of Glomerular Filtration
 Three mechanisms control the GFR
 Renal autoregulation (intrinsic system)
 Neural controls
 Hormonal mechanism (the renin-angiotensin
system)

Intrinsic Controls
 Under normal conditions, renal autoregulation
maintains a nearly constant glomerular filtration
rate
 Autoregulation entails two types of control
 Myogenic – responds to changes in pressure in the
renal blood vessels
 Flow-dependent tubuloglomerular feedback –
senses changes in the juxtaglomerular apparatus

Extrinsic Controls
 When the sympathetic nervous system is at rest:
 Renal blood vessels are maximally dilated
 Autoregulation mechanisms prevail (takes over)

Extrinsic Controls
 Under stress:
 Norepinephrine is released by the sympathetic
nervous system
 Epinephrine is released by the adrenal medulla
 Afferent arterioles constrict and filtration is
inhibited
 The sympathetic nervous system also stimulates
the renin-angiotensin mechanism

Renin-Angiotensin Mechanism
 Is triggered when the JG cells release renin
 Renin acts on angiotensinogen to release
angiotensin I
 Angiotensin I is converted to angiotensin II
 Angiotensin II:
 Causes mean arterial pressure to rise
 Stimulates the adrenal cortex to release aldosterone
 As a result, both systemic and glomerular
hydrostatic pressure rise

Renin Release
 Renin release is triggered by:
 Reduced stretch of the granular JG cells
 Stimulation of the JG cells by activated macula
densa cells
 Direct stimulation of the JG cells via 1-adrenergic
receptors by renal nerves
 Angiotensin II

Renin Release
Figure 25.10

Other Factors Affecting Glomerular Filtration
 Prostaglandins (PGE2 and PGI2)
 Vasodilators produced in response to sympathetic
stimulation and angiotensin II
 Are thought to prevent renal damage when
peripheral resistance is increased
 Nitric oxide – vasodilator produced by the vascular
endothelium
 Adenosine – vasoconstrictor of renal vasculature
 Endothelin – a powerful vasoconstrictor secreted
by tubule cells

Human
Anatomy
& Physiology
SEVENTH EDITION
Elaine N. Marieb
Katja Hoehn
Bluegrass Technical
CHAPTER
25The Urinary
System
P A R T B

Tubular Reabsorption
 A transepithelial process whereby most tubule
contents are returned to the blood
 Transported substances move through three
membranes
 Luminal and basolateral membranes of tubule cells
 Endothelium of peritubular capillaries
 Only Ca2+, Mg2+, K+, and some Na+ are reabsorbed
via paracellular pathways

Tubular Reabsorption
 All organic nutrients are reabsorbed
 Water and ion reabsorption is hormonally
controlled
 Reabsorption may be an active (requiring ATP) or
passive process

Sodium Reabsorption:
Primary Active Transport
 Sodium reabsorption is almost always by active
transport
 Na+ enters the tubule cells at the luminal
membrane
 Is actively transported out of the tubules by a
Na+-K+ ATPase pump

Sodium Reabsorption:
Primary Active Transport
 From there it moves to peritubular capillaries due
to:
 Low hydrostatic pressure
 High osmotic pressure of the blood
 Na+ reabsorption provides the energy and the
means for reabsorbing most other solutes

Routes of Water and Solute Reabsorption
Figure 25.11

Reabsorption by PCT Cells
 Active pumping of Na+ drives reabsorption of:
 Water by osmosis, aided by water-filled pores
called aquaporins
 Cations and fat-soluble substances by diffusion
 Organic nutrients and selected cations by
secondary active transport

Reabsorption by PCT Cells
PLAY InterActive Physiology ®: Early Filtrate Processing, pages 3–15
Figure 25.12

Nonreabsorbed Substances
 A transport maximum (Tm):
 Reflects the number of carriers in the renal tubules
available
 Exists for nearly every substance that is actively
reabsorbed
 When the carriers are saturated, excess of that
substance is excreted

Nonreabsorbed Substances
 Substances are not reabsorbed if they:
 Lack carriers
 Are not lipid soluble
 Are too large to pass through membrane pores
 Urea, creatinine, and uric acid are the most
important nonreabsorbed substances

Absorptive Capabilities of Renal Tubules and
Collecting Ducts
 Substances reabsorbed in PCT include:
 Sodium, all nutrients, cations, anions, and water
 Urea and lipid-soluble solutes
 Small proteins
 Loop of Henle reabsorbs:
 H2O, Na+, Cl, K+ in the descending limb
 Ca2+, Mg2+, and Na+ in the ascending limb

Absorptive Capabilities of Renal Tubules and
Collecting Ducts
 DCT absorbs:
 Ca2+, Na+, H+, K+, and water
 HCO3
 and Cl
 Collecting duct absorbs:
 Water and urea

Na+ Entry into Tubule Cells
 Passive entry: Na+-K+ ATPase pump
 In the PCT: facilitated diffusion using symport and
antiport carriers
 In the ascending loop of Henle: facilitated
diffusion via Na+-K+-2Cl symport system
 In the DCT: Na+-Cl– symporter
 In collecting tubules: diffusion through membrane
pores

Atrial Natriuretic Peptide Activity
 ANP reduces blood Na+ which:
 Decreases blood volume
 Lowers blood pressure
 ANP lowers blood Na+ by:
 Acting directly on medullary ducts to inhibit Na+
reabsorption
 Counteracting the effects of angiotensin II
 Indirectly stimulating an increase in GFR reducing
water reabsorption

Tubular Secretion
 Essentially reabsorption in reverse, where
substances move from peritubular capillaries or
tubule cells into filtrate
 Tubular secretion is important for:
 Disposing of substances not already in the filtrate
 Eliminating undesirable substances such as urea
and uric acid
 Ridding the body of excess potassium ions
 Controlling blood pH

Regulation of Urine Concentration and
Volume
 Osmolality
 The number of solute particles dissolved in 1L of
water
 Reflects the solution’s ability to cause osmosis
 Body fluids are measured in milliosmols (mOsm)
 The kidneys keep the solute load of body fluids
constant at about 300 mOsm
 This is accomplished by the countercurrent
mechanism

Countercurrent Mechanism
 Interaction between the flow of filtrate through the
loop of Henle (countercurrent multiplier) and the
flow of blood through the vasa recta blood vessels
(countercurrent exchanger)
 The solute concentration in the loop of Henle
ranges from 300 mOsm to 1200 mOsm
 Dissipation of the medullary osmotic gradient is
prevented because the blood in the vasa recta
equilibrates with the interstitial fluid

Osmotic Gradient in the Renal Medulla
Figure 25.13

Loop of Henle: Countercurrent Multiplier
 The descending loop of Henle:
 Is relatively impermeable to solutes
 Is permeable to water
 The ascending loop of Henle:
 Is permeable to solutes
 Is impermeable to water
 Collecting ducts in the deep medullary regions are
permeable to urea

Loop of Henle: Countercurrent Exchanger
 The vasa recta is a countercurrent exchanger that:
 Maintains the osmotic gradient
 Delivers blood to the cells in the area
Early Filtrate Processing, pages 16–21

Loop of Henle: Countercurrent Mechanism
Figure 25.14

Formation of Dilute Urine
 Filtrate is diluted in the ascending loop of Henle
 Dilute urine is created by allowing this filtrate to
continue into the renal pelvis
 This will happen as long as antidiuretic hormone
(ADH) is not being secreted

Formation of Dilute Urine
 Collecting ducts remain impermeable to water; no
further water reabsorption occurs
 Sodium and selected ions can be removed by
active and passive mechanisms
 Urine osmolality can be as low as 50 mOsm (one-
sixth that of plasma)

Formation of Concentrated Urine
 Antidiuretic hormone (ADH) inhibits diuresis
 This equalizes the osmolality of the filtrate and the
interstitial fluid
 In the presence of ADH, 99% of the water in
filtrate is reabsorbed

Late Filtrate Processing, pages 3–12
Formation of Concentrated Urine
 ADH-dependent water reabsorption is called
facultative water reabsorption
 ADH is the signal to produce concentrated urine
 The kidneys’ ability to respond depends upon the
high medullary osmotic gradient

Formation of Dilute and Concentrated Urine
Figure 25.15a, b

Diuretics
 Chemicals that enhance the urinary output include:
 Any substance not reabsorbed
 Substances that exceed the ability of the renal
tubules to reabsorb it
 Substances that inhibit Na+ reabsorption

Diuretics
 Osmotic diuretics include:
 High glucose levels – carries water out with the
glucose
 Alcohol – inhibits the release of ADH
 Caffeine and most diuretic drugs – inhibit sodium
ion reabsorption
 Lasix and Diuril – inhibit Na+-associated
symporters

Summary of Nephron Function
Figure 25.16

Renal Clearance
 The volume of plasma that is cleared of a
particular substance in a given time
 Renal clearance tests are used to:
 Determine the GFR
 Detect glomerular damage
 Follow the progress of diagnosed renal disease

Renal Clearance
RC = UV/P
RC = renal clearance rate
U = concentration (mg/ml) of the substance in
urine
V = flow rate of urine formation (ml/min)
P = concentration of the same substance in plasma

Physical Characteristics of Urine
 Color and transparency
 Clear, pale to deep yellow (due to urochrome)
 Concentrated urine has a deeper yellow color
 Drugs, vitamin supplements, and diet can change
the color of urine
 Cloudy urine may indicate infection of the urinary
tract

 Odor
 Fresh urine is slightly aromatic
 Standing urine develops an ammonia odor
 Some drugs and vegetables (asparagus) alter the
usual odor

 pH
 Slightly acidic (pH 6) with a range of 4.5 to 8.0
 Diet can alter pH
 Specific gravity
 Is dependent on solute concentration

Chemical Composition of Urine
 Urine is 95% water and 5% solutes
 Nitrogenous wastes: urea, uric acid, and creatinine
 Other normal solutes include:
 Sodium, potassium, phosphate, and sulfate ions
 Calcium, magnesium, and bicarbonate ions
 Abnormally high concentrations of any urinary
constituents may indicate pathology

Ureters
 Slender tubes that convey urine from the kidneys
to the bladder
 Ureters enter the base of the bladder through the
posterior wall
 This closes their distal ends as bladder pressure
increases and prevents backflow of urine into the
ureters

Ureters
 Ureters have a trilayered wall
 Transitional epithelial mucosa
 Smooth muscle muscularis
 Fibrous connective tissue adventitia
 Ureters actively propel urine to the bladder via
response to smooth muscle stretch

Urinary Bladder
 Smooth, collapsible, muscular sac that stores urine
 It lies retroperitoneally on the pelvic floor posterior
to the pubic symphysis
 Males – prostate gland surrounds the neck
inferiorly
 Females – anterior to the vagina and uterus
 Trigone – triangular area outlined by the openings
for the ureters and the urethra
 Clinically important because infections tend to
persist in this region

Urinary Bladder
 The bladder wall has three layers
 Transitional epithelial mucosa
 A thick muscular layer
 A fibrous adventitia
 The bladder is distensible and collapses when
empty
 As urine accumulates, the bladder expands without
significant rise in internal pressure

Urinary Bladder
Figure 25.18a, b

Urethra
 Muscular tube that:
 Drains urine from the bladder
 Conveys it out of the body

Urethra
 Sphincters keep the urethra closed when urine is
not being passed
 Internal urethral sphincter – involuntary sphincter
at the bladder-urethra junction
 External urethral sphincter – voluntary sphincter
surrounding the urethra as it passes through the
urogenital diaphragm
 Levator ani muscle – voluntary urethral sphincter

Urethra
 The female urethra is tightly bound to the anterior
vaginal wall
 Its external opening lies anterior to the vaginal
opening and posterior to the clitoris
 The male urethra has three named regions
 Prostatic urethra – runs within the prostate gland
 Membranous urethra – runs through the urogenital
diaphragm
 Spongy (penile) urethra – passes through the penis
and opens via the external urethral orifice

Urethra
Figure 25.18a, b

Micturition (Voiding or Urination)
 The act of emptying the bladder
 Distension of bladder walls initiates spinal reflexes
that:
 Stimulate contraction of the external urethral
sphincter
 Inhibit the detrusor muscle and internal sphincter
(temporarily)
 Voiding reflexes:
 Stimulate the detrusor muscle to contract
 Inhibit the internal and external sphincters

Neural Circuits Controlling Micturition
Figure 25.20a, b

Human
Anatomy
& Physiology
SEVENTH EDITION
Elaine N. Marieb
Katja Hoehn
Bluegrass Technical
CHAPTER
26Fluid,
Electrolyte,
and Acid-Base
Balance

Body Water Content
 Infants have low body fat, low bone mass, and are
73% or more water
 Total water content declines throughout life
 Healthy males are about 60% water; healthy
females are around 50%

Body Water Content
 This difference reflects females’:
 Higher body fat
 Smaller amount of skeletal muscle
 In old age, only about 45% of body weight is water

Fluid Compartments
 Water occupies two main fluid compartments
 Intracellular fluid (ICF) – about two thirds by
volume, contained in cells
 Extracellular fluid (ECF) – consists of two major
subdivisions
 Plasma – the fluid portion of the blood
 Interstitial fluid (IF) – fluid in spaces between cells
 Other ECF – lymph, cerebrospinal fluid, eye
humors, synovial fluid, serous fluid, and
gastrointestinal secretions

Fluid Compartments
Introduction to Body Fluids, page 10
Figure 26.1

Composition of Body Fluids
 Water is the universal solvent
 Solutes are broadly classified into:
 Electrolytes – inorganic salts, all acids and bases,
and some proteins
 Nonelectrolytes – examples include glucose, lipids,
creatinine, and urea
 Electrolytes have greater osmotic power than
nonelectrolytes
 Water moves according to osmotic gradients

Electrolyte Concentration
 Expressed in milliequivalents per liter (mEq/L), a
measure of the number of electrical charges in one
liter of solution
 mEq/L = (concentration of ion in [mg/L]/the
atomic weight of ion)  number of electrical
charges on one ion
 For single charged ions, 1 mEq = 1 mOsm
 For bivalent ions, 1 mEq = 1/2 mOsm

Extracellular and Intracellular Fluids
 Each fluid compartment of the body has a
distinctive pattern of electrolytes
 Extracellular fluids are similar (except for the high
protein content of plasma)
 Sodium is the chief cation
 Chloride is the major anion
 Intracellular fluids have low sodium and chloride
 Potassium is the chief cation
 Phosphate is the chief anion

 Sodium and potassium concentrations in extra- and
intracellular fluids are nearly opposites
 This reflects the activity of cellular ATP-
dependent sodium-potassium pumps
 Electrolytes determine the chemical and physical
reactions of fluids

 Proteins, phospholipids, cholesterol, and neutral
fats account for:
 90% of the mass of solutes in plasma
 60% of the mass of solutes in interstitial fluid
 97% of the mass of solutes in the intracellular
compartment

Fluid Movement Among Compartments
 Compartmental exchange is regulated by osmotic
and hydrostatic pressures
 Net leakage of fluid from the blood is picked up by
lymphatic vessels and returned to the bloodstream
 Exchanges between interstitial and intracellular
fluids are complex due to the selective
permeability of the cellular membranes
 Two-way water flow is substantial

 Ion fluxes are restricted and move selectively by
active transport
 Nutrients, respiratory gases, and wastes move
unidirectionally
 Plasma is the only fluid that circulates throughout
the body and links external and internal
environments
 Osmolalities of all body fluids are equal; changes
in solute concentrations are quickly followed by
osmotic changes
Introduction to Body Fluids, pages 19–22

Water Balance and ECF Osmolality
 To remain properly hydrated, water intake must
equal water output
 Water intake sources
 Ingested fluid (60%) and solid food (30%)
 Metabolic water or water of oxidation (10%)

Water Balance and ECF Osmolality
 Water output
 Urine (60%) and feces (4%)
 Insensible losses (28%), sweat (8%)
 Increases in plasma osmolality trigger thirst and
release of antidiuretic hormone (ADH)

Regulation of Water Output
 Obligatory water losses include:
 Insensible water losses from lungs and skin
 Water that accompanies undigested food residues
in feces
 Obligatory water loss reflects the fact that:
 Kidneys excrete 900-1200 mOsm of solutes to
maintain blood homeostasis
 Urine solutes must be flushed out of the body in
water
Water Homeostasis, pages 3–10

Influence and Regulation of ADH
 Water reabsorption in collecting ducts is proportional to
ADH release
 Low ADH levels produce dilute urine and reduced volume
of body fluids
 High ADH levels produce concentrated urine
 Hypothalamic osmoreceptors trigger or inhibit ADH
release
 Factors that specifically trigger ADH release include
prolonged fever; excessive sweating, vomiting, or diarrhea;
severe blood loss; and traumatic burns

Mechanisms and Consequences of ADH
Release
Figure 26.6

Disorders of Water Balance: Dehydration
 Water loss exceeds water intake and the body is in
negative fluid balance
 Causes include: hemorrhage, severe burns, prolonged
vomiting or diarrhea, profuse sweating, water
deprivation, and diuretic abuse
 Signs and symptoms: thirst, dry flushed skin, and
oliguria (low output of urine, output below 300-
500ml/day)
 Prolonged dehydration may lead to weight loss, fever,
and mental confusion
 Other consequences include hypovolemic shock and
loss of electrolytes

Disorders of Water Balance:
Hypotonic Hydration
 Renal insufficiency or an extraordinary amount of
water ingested quickly can lead to cellular
overhydration, or water intoxication
 ECF is diluted – sodium content is normal but
excess water is present
 The resulting hyponatremia promotes net osmosis
into tissue cells, causing swelling
 These events must be quickly reversed to prevent
severe metabolic disturbances, particularly in
neurons

Disorders of Water Balance: Edema
 Atypical accumulation of fluid in the interstitial
space, leading to tissue swelling
 Caused by anything that increases flow of fluids
out of the bloodstream or hinders their return
 Factors that accelerate fluid loss include:
 Increased blood pressure, capillary permeability
 Incompetent venous valves, localized blood vessel
blockage
 Congestive heart failure, hypertension, high blood
volume

Edema
 Hindered fluid return usually reflects an imbalance in
colloid osmotic pressures (a form of osmotic pressure
exerted by proteins in blood plasma that usually tends to
pull water into the circulatory system)
 Hypoproteinemia – low levels of plasma proteins
 Forces fluids out of capillary beds at the arterial ends
 Fluids fail to return at the venous ends
 Results from protein malnutrition, liver disease, or
glomerulonephritis

Edema
 Blocked (or surgically removed) lymph vessels:
 Cause leaked proteins to accumulate in interstitial
fluid
 Exert increasing colloid osmotic pressure, which
draws fluid from the blood
 Interstitial fluid accumulation results in low blood
pressure and severely impaired circulation

Electrolyte Balance
 Electrolytes are salts, acids, and bases, but
electrolyte balance usually refers only to salt
balance
 Salts are important for:
 Neuromuscular excitability
 Secretory activity
 Membrane permeability
 Controlling fluid movements
 Salts enter the body by ingestion and are lost via
perspiration, feces, and urine

Sodium in Fluid and Electrolyte Balance
 Sodium holds a central position in fluid and
electrolyte balance
 Sodium salts:
 Account for 90-95% of all solutes in the ECF
 Contribute 280 mOsm of the total 300 mOsm ECF
solute concentration
 Sodium is the single most abundant cation in the
ECF
 Sodium is the only cation exerting significant
osmotic pressure

 The role of sodium in controlling ECF volume and
water distribution in the body is a result of:
 Sodium being the only cation to exert significant
osmotic pressure
 Sodium ions leaking into cells and being pumped
out against their electrochemical gradient
 Sodium concentration in the ECF normally
remains stable

 Changes in plasma sodium levels affect:
 Plasma volume, blood pressure
 ICF and interstitial fluid volumes
 Renal acid-base control mechanisms are coupled to
sodium ion transport
Electrolyte Homeostasis, pages 4–6, 18–22

Regulation of Sodium Balance: Aldosterone
 Sodium reabsorption
 65% of sodium in filtrate is reabsorbed in the
proximal tubules
 25% is reclaimed in the loops of Henle
 When aldosterone levels are high, all remaining
Na+ is actively reabsorbed
 Water follows sodium if tubule permeability has
been increased with ADH

 The renin-angiotensin mechanism triggers the
release of aldosterone
 This is mediated by the juxtaglomerular apparatus,
which releases renin in response to:
 Sympathetic nervous system stimulation
 Decreased filtrate osmolality
 Decreased stretch (due to decreased blood
pressure)
 Renin catalyzes the production of angiotensin II,
which prompts aldosterone release

 Adrenal cortical cells are directly stimulated to
release aldosterone by elevated K+ levels in the
ECF
 Aldosterone brings about its effects (diminished
urine output and increased blood volume) slowly

Figure 26.8

Cardiovascular System Baroreceptors
 Baroreceptors alert the brain of increases in blood
volume (hence increased blood pressure)
 Sympathetic nervous system impulses to the
kidneys decline
 Afferent arterioles dilate
 Glomerular filtration rate rises
 Sodium and water output increase

Cardiovascular System Baroreceptors
 This phenomenon, called pressure diuresis,
decreases blood pressure
 Drops in systemic blood pressure lead to opposite
actions and systemic blood pressure increases
 Since sodium ion concentration determines fluid
volume, baroreceptors can be viewed as “sodium
receptors”

Maintenance of Blood Pressure Homeostasis
Figure 26.9

Atrial Natriuretic Peptide (ANP)
 Reduces blood pressure and blood volume by
inhibiting:
 Events that promote vasoconstriction
 Na+ and water retention
 Is released in the heart atria as a response to stretch
(elevated blood pressure)
 Has potent diuretic and natriuretic effects
 Promotes excretion of sodium and water
 Inhibits angiotensin II production

Mechanisms and Consequences of ANP
Release
Figure 26.10

Influence of Other Hormones on Sodium
Balance
 Estrogens:
 Enhance NaCl reabsorption by renal tubules
 May cause water retention during menstrual cycles
 Are responsible for edema during pregnancy

Influence of Other Hormones on Sodium
Balance
 Progesterone:
 Decreases sodium reabsorption
 Acts as a diuretic, promoting sodium and water
loss
 Glucocorticoids – enhance reabsorption of sodium
and promote edema

Regulation of Potassium Balance
 Relative ICF-ECF potassium ion concentration
affects a cell’s resting membrane potential
 Excessive ECF potassium decreases membrane
potential
 Too little K+ causes hyperpolarization and
nonresponsiveness

Regulation of Potassium Balance
 Hyperkalemia and hypokalemia can:
 Disrupt electrical conduction in the heart
 Lead to sudden death
 Hydrogen ions shift in and out of cells
 Leads to corresponding shifts in potassium in the
opposite direction
 Interferes with activity of excitable cells

Regulatory Site: Cortical Collecting Ducts
 Less than 15% of filtered K+ is lost to urine
regardless of need
 K+ balance is controlled in the cortical collecting
ducts by changing the amount of potassium secreted
into filtrate
 Excessive K+ is excreted over basal levels by cortical
collecting ducts
 When K+ levels are low, the amount of secretion and
excretion is kept to a minimum
 Type A intercalated cells can reabsorb some K+ left
in the filtrate

Influence of Plasma Potassium Concentration
 High K+ content of ECF favors principal cells to
secrete K+
 Low K+ or accelerated K+ loss depresses its
secretion by the collecting ducts
Electrolyte Homeostasis, pages 28–32

Influence of Aldosterone
 Aldosterone stimulates potassium ion secretion by
principal cells
 In cortical collecting ducts, for each Na+
reabsorbed, a K+ is secreted
 Increased K+ in the ECF around the adrenal cortex
causes:
 Release of aldosterone
 Potassium secretion
 Potassium controls its own ECF concentration via
feedback regulation of aldosterone release

Regulation of Calcium
 Ionic calcium in ECF is important for:
 Blood clotting
 Cell membrane permeability
 Secretory behavior
 Hypocalcemia:
 Increases excitability
 Causes muscle tetany

Regulation of Calcium
 Hypercalcemia:
 Inhibits neurons and muscle cells
 May cause heart arrhythmias
 Calcium balance is controlled by parathyroid
hormone (PTH) and calcitonin

Regulation of Calcium and Phosphate
 PTH promotes increase in calcium levels by
targeting:
 Bones – PTH activates osteoclasts to break down
bone matrix
 Small intestine – PTH enhances intestinal
absorption of calcium
 Kidneys – PTH enhances calcium reabsorption and
decreases phosphate reabsorption
 Calcium reabsorption and phosphate excretion go
hand in hand

Regulation of Calcium and Phosphate
 Filtered phosphate is actively reabsorbed in the
proximal tubules
 In the absence of PTH, phosphate reabsorption is
regulated by its transport maximum and excesses are
excreted in urine
 High or normal ECF calcium levels inhibit PTH
secretion
 Release of calcium from bone is inhibited
 Larger amounts of calcium are lost in feces and urine
 More phosphate is retained

Influence of Calcitonin
 Released in response to rising blood calcium levels
 Calcitonin is a PTH antagonist, but its contribution
to calcium and phosphate homeostasis is minor to
negligible
Electrolyte Homeostasis, pages 33–37

Regulation of Anions
 Chloride is the major anion accompanying sodium
in the ECF
 99% of chloride is reabsorbed under normal pH
conditions
 When acidosis occurs, fewer chloride ions are
reabsorbed
 Other anions have transport maximums and
excesses are excreted in urine

Acid-Base Balance
 Normal pH of body fluids
 Arterial blood is 7.4
 Venous blood and interstitial fluid is 7.35
 Intracellular fluid is 7.0
 Alkalosis or alkalemia – arterial blood pH rises
above 7.45
 Acidosis or acidemia – arterial pH drops below
7.35 (physiological acidosis)

Sources of Hydrogen Ions
 Most hydrogen ions originate from cellular
metabolism
 Breakdown of phosphorus-containing proteins
releases phosphoric acid into the ECF
 Anaerobic respiration of glucose produces lactic
acid
 Fat metabolism yields organic acids and ketone
bodies
 Transporting carbon dioxide as bicarbonate
releases hydrogen ions

Hydrogen Ion Regulation
 Concentration of hydrogen ions is regulated
sequentially by:
 Chemical buffer systems – act within seconds
 The respiratory center in the brain stem – acts
within 1-3 minutes
 Renal mechanisms – require hours to days to effect
pH changes

Chemical Buffer Systems
 Strong acids – all their H+ is dissociated
completely in water
 Weak acids – dissociate partially in water and are
efficient at preventing pH changes
 Strong bases – dissociate easily in water and
quickly tie up H+
 Weak bases – accept H+ more slowly (e.g., HCO3
¯
and NH3)
Acid/Base Homeostasis, pages 3–10

Strong and Weak Acids
Figure 26.11

Chemical Buffer Systems
 One or two molecules that act to resist pH changes
when strong acid or base is added
 Three major chemical buffer systems
 Bicarbonate buffer system
 Phosphate buffer system
 Protein buffer system
 Any drifts in pH are resisted by the entire chemical
buffering system

Bicarbonate Buffer System
 A mixture of carbonic acid (H2CO3) and its salt,
sodium bicarbonate (NaHCO3) (potassium or
magnesium bicarbonates work as well)
 If strong acid is added:
 Hydrogen ions released combine with the
bicarbonate ions and form carbonic acid (a weak
acid)
 The pH of the solution decreases only slightly

Bicarbonate Buffer System
 If strong base is added:
 It reacts with the carbonic acid to form sodium
bicarbonate (a weak base)
 The pH of the solution rises only slightly
 This system is the only important ECF buffer
Acid/Base Homeostasis, pages 16–17

Phosphate Buffer System
 Nearly identical to the bicarbonate system
 Its components are:
 Sodium salts of dihydrogen phosphate (H2PO4
¯), a
weak acid
 Monohydrogen phosphate (HPO4
2¯), a weak base
 This system is an effective buffer in urine and
intracellular fluid

Protein Buffer System
 Plasma and intracellular proteins are the body’s
most plentiful and powerful buffers
 Some amino acids of proteins have:
 Free organic acid groups (weak acids)
 Groups that act as weak bases (e.g., amino groups)
 Amphoteric molecules are protein molecules that
can function as both a weak acid and a weak base
Acid/Base Homeostasis, page 19

Physiological Buffer Systems
 The respiratory system regulation of acid-base
balance is a physiological buffering system
 There is a reversible equilibrium between:
 Dissolved carbon dioxide and water
 Carbonic acid and the hydrogen and bicarbonate
ions
CO2 + H2O  H2CO3  H+ + HCO3¯
Acid/Base Homeostasis, page 20–26

Physiological Buffer Systems
 During carbon dioxide unloading, hydrogen ions are
incorporated into water
 When hypercapnia or rising plasma H+ occurs:
 Deeper and more rapid breathing expels more carbon dioxide
 Hydrogen ion concentration is reduced
 Alkalosis causes slower, more shallow breathing, causing H+
to increase
 Respiratory system impairment causes acid-base imbalance
(respiratory acidosis or respiratory alkalosis)

Renal Mechanisms of Acid-Base Balance
 Chemical buffers can tie up excess acids or bases,
but they cannot eliminate them from the body
 The lungs can eliminate carbonic acid by
eliminating carbon dioxide
 Only the kidneys can rid the body of metabolic
acids (phosphoric, uric, and lactic acids and
ketones) and prevent metabolic acidosis
 The ultimate acid-base regulatory organs are the
kidneys

 The most important renal mechanisms for
regulating acid-base balance are:
 Conserving (reabsorbing) or generating new
bicarbonate ions
 Excreting bicarbonate ions
 Losing a bicarbonate ion is the same as gaining a
hydrogen ion; reabsorbing a bicarbonate ion is the
same as losing a hydrogen ion

 Hydrogen ion secretion occurs in the PCT and in
type A intercalated cells
 Hydrogen ions come from the dissociation of
carbonic acid

Reabsorption of Bicarbonate
 Carbon dioxide combines with water in tubule
cells, forming carbonic acid
 Carbonic acid splits into hydrogen ions and
bicarbonate ions
 For each hydrogen ion secreted, a sodium ion and
a bicarbonate ion are reabsorbed by the PCT cells
 Secreted hydrogen ions form carbonic acid; thus,
bicarbonate disappears from filtrate at the same
rate that it enters the peritubular capillary blood

Reabsorption of Bicarbonate
 Carbonic acid formed
in filtrate dissociates
to release carbon
dioxide and water
 Carbon dioxide then
diffuses into tubule
cells, where it acts to
trigger further
hydrogen ion
secretion
Figure 26.12

Generating New Bicarbonate Ions
 Two mechanisms carried out by type A
intercalated cells generate new bicarbonate ions
 Both involve renal excretion of acid via secretion
and excretion of hydrogen ions or ammonium ions
(NH4
+)

Hydrogen Ion Excretion
 Dietary hydrogen ions must be counteracted by
generating new bicarbonate
 The excreted hydrogen ions must bind to buffers in
the urine (phosphate buffer system)
 Intercalated cells actively secrete hydrogen ions
into urine, which is buffered and excreted
 Bicarbonate generated is:
 Moved into the interstitial space via a cotransport
system
 Passively moved into the peritubular capillary
blood

Hydrogen Ion Excretion
 In response to
acidosis:
 Kidneys generate
bicarbonate ions
and add them to the
blood
 An equal amount of
hydrogen ions are
added to the urine
Figure 26.13

Ammonium Ion Excretion
 This method uses ammonium ions produced by the
metabolism of glutamine in PCT cells
 Each glutamine metabolized produces two
ammonium ions and two bicarbonate ions
 Bicarbonate moves to the blood and ammonium
ions are excreted in urine

Ammonium Ion Excretion
Figure 26.14

Bicarbonate Ion Secretion
 When the body is in alkalosis, type B intercalated
cells:
 Exhibit bicarbonate ion secretion
 Reclaim hydrogen ions and acidify the blood
 The mechanism is the opposite of type A
intercalated cells and the bicarbonate ion
reabsorption process
 Even during alkalosis, the nephrons and collecting
ducts excrete fewer bicarbonate ions than they
conserve

Respiratory Acidosis and Alkalosis
 Result from failure of the respiratory system to
balance pH
 PCO2 is the single most important indicator of
respiratory inadequacy
 PCO2 levels
 Normal PCO2 fluctuates between 35 and 45 mm Hg
 Values above 45 mm Hg signal respiratory acidosis
 Values below 35 mm Hg indicate respiratory
alkalosis

Respiratory Acidosis and Alkalosis
 Respiratory acidosis is the most common cause of
acid-base imbalance
 Occurs when a person breathes shallowly, or gas
exchange is hampered by diseases such as
pneumonia, cystic fibrosis, or emphysema
 Respiratory alkalosis is a common result of
hyperventilation

Metabolic Acidosis
 All pH imbalances except those caused by
abnormal blood carbon dioxide levels
 Metabolic acid-base imbalance – bicarbonate ion
levels above or below normal (22-26 mEq/L)
 Metabolic acidosis is the second most common
cause of acid-base imbalance
 Typical causes are ingestion of too much alcohol
and excessive loss of bicarbonate ions
 Other causes include accumulation of lactic acid,
shock, ketosis in diabetic crisis, starvation, and
kidney failure

Metabolic Alkalosis
 Rising blood pH and bicarbonate levels indicate
metabolic alkalosis
 Typical causes are:
 Vomiting of the acid contents of the stomach
 Intake of excess base (e.g., from antacids)
 Constipation, in which excessive bicarbonate is
reabsorbed

Respiratory and Renal Compensations
 Acid-base imbalance due to inadequacy of a
physiological buffer system is compensated for by
the other system
 The respiratory system will attempt to correct
metabolic acid-base imbalances
 The kidneys will work to correct imbalances
caused by respiratory disease

Respiratory Compensation
 In metabolic acidosis:
 The rate and depth of breathing are elevated
 Blood pH is below 7.35 and bicarbonate level is
low
 As carbon dioxide is eliminated by the respiratory
system, PCO2 falls below normal
 In respiratory acidosis, the respiratory rate is often
depressed and is the immediate cause of the
acidosis

Respiratory Compensation
 In metabolic alkalosis:
 Compensation exhibits slow, shallow breathing,
allowing carbon dioxide to accumulate in the blood
 Correction is revealed by:
 High pH (over 7.45) and elevated bicarbonate ion
levels
 Rising PCO2

Renal Compensation
 To correct respiratory acid-base imbalance, renal
mechanisms are stepped up
 Acidosis has high PCO2 and high bicarbonate levels
 The high PCO2 is the cause of acidosis
 The high bicarbonate levels indicate the kidneys
are retaining bicarbonate to offset the acidosis

Renal Compensation
 Alkalosis has Low PCO2 and high pH
 The kidneys eliminate bicarbonate from the body
by failing to reclaim it or by actively secreting it

Developmental Aspects
 Water content of the body is greatest at birth (70-
80%) and declines until adulthood, when it is about
58%
 At puberty, sexual differences in body water
content arise as males develop greater muscle mass
 Homeostatic mechanisms slow down with age
 Elders may be unresponsive to thirst clues and are
at risk of dehydration
 The very young and the very old are the most
frequent victims of fluid, acid-base, and electrolyte
imbalances

Problems with Fluid, Electrolyte, and Acid-
Base Balance
 Occur in the young, reflecting:
 Low residual lung volume
 High rate of fluid intake and output
 High metabolic rate yielding more metabolic
wastes
 High rate of insensible water loss
 Inefficiency of kidneys in infants

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