Urinary System Part Three

Questions?
 Homework due in lab 6
 PreLab #6
 HW 15 & 16 (follow directions, 6 points!)
Part 3
Variations in Urine Formation
 Composition varies
 Fluid volume
 Solute concentration
Variations in Urine Formation
 Water intake must equal water loss
 Kidney regulates water loss by producing:


Hypotonic urine (dilute)
Hypertonic urine (concentrated)
Countercurrent Mechanism
 Role of countercurrent mechanisms
 Establish and maintain an osmotic gradient
 Creates hypertonic interstitial fluid within kidney
medulla
 Hypertonic interstitial fluid allows the kidneys to vary
urine concentration
Osmolality
of interstitial
fluid
(mOsm)
Active transport
H2O
NaCI
H2O
NaCI
H2O
NaCI
H2O
NaCI
Cortex
Passive transport
Water impermeable
Countercurrent multiplier
The long loops of Henle of the
juxtamedullary nephrons
create the medullary
osmotic gradient.
Outer
medulla
H2O
NaCI
H2O
H2O
Inner
medulla
Loop of Henle
Figure 25.16a
Formation of Concentrated Urine
 Depends on the medullary osmotic gradient and the
ability to alter permeability of the collecting tubules
 ADH triggers reabsorption of H2O in the collecting
tubules
 Osmotic gradient drives water from filtrate into blood
Active transport
Passive transport
Collecting duct
H2O
Descending limb
of loop of Henle
DCT
H2O
Cortex
NaCI
H2O
H2O
H2O
NaCI
Outer
medulla
NaCI
H2O
Inner
medulla
(b) Maximal ADH
H2O
Urea
H2O
Urea
H2O
Small volume of
concentrated urine
Figure 25.17b
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
Active transport
Passive transport
Collecting duct
Descending limb
of loop of Henle
DCT
Cortex
NaCI
H2O
NaCI
Outer
medulla
NaCI
H2O
Urea
Inner
medulla
(a) Absence of ADH
Large volume
of dilute urine
Figure 25.17a
Regulation of Water Output
 Influence of ADH
 Water reabsorption in collecting tubules is dependent
upon ADH release
  ADH  dilute urine and  volume of body fluids
  ADH  concentrated urine
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
Acid-Base Balance
 pH affects all functional proteins and biochemical
reactions in the body
 Regulation prevents changes in body’s internal environment
 Alkalosis or alkalemia: arterial blood pH >7.45
 Acidosis or acidemia: arterial pH < 7.35
Acid-Base Balance
 Concentration of hydrogen ions is regulated by
1. Chemical buffer systems

Rapid, first line of defense
Brainstem respiratory centers
2.

Acts within 1–3 minutes
Renal mechanisms
3.


Most potent
Requires hours to days to affect pH changes
Acid-Base Balance
 Lungs

Regulate carbonic acid levels by CO2 manipulation
 Kidneys

Selectively secrete and reabsorb to maintain pH
Acid-Base Balance
 Most important renal mechanisms:
 Conserving (reabsorbing) HCO3–
 Excreting HCO3–
 Secretion of H+

H+ secretion occurs in the PCT and in collecting tubules
Acid-Base Balance
 Examples
 Respiratory Acidosis

Kidneys
 Respiratory Alkalosis
 Kidneys
More on Compensation…
 Uncompensated
 pH abnormal and either CO2 or HCO3- is off
 The other system has not started to compensate at all
 Partially compensated
 pH is abnormal and both CO2 and HCO3- are off
 The other system is trying to compensate
 Fully compensated
 pH is normal and both CO2 and HCO3- are off
 The other system has corrected the pH but there is still and acid
base imbalance since CO2 and HCO3- are abnormal
Lets practice…Urinary 31 #21 - 24
Variations in Blood Pressure
 Activity of kidney related to variations in blood pressure
 Blood pressure and blood volume are related
 Blood volume is controlled by


Solute concentration
Water regulation
Variations in Blood Pressure
 Renal mechanisms influencing blood pressure
 ADH

Water
 Renin-angiotensin mechanism


Sodium
Potassium
Antidiuretic Hormone (ADH)
 Plasma osmolarity
Increase → osmoreceptors stimulated → thirst & ADH secretion →
water reabsorption (decreased urine output) →
increased blood volume → increased blood pressure

Causes?
Aldosterone
 Aldosterone stimulates K+ secretion and Na+
reabsorption
 Changes in plasma sodium levels affect
 Plasma volume, blood pressure
Aldosterone
 Regulation of sodium balance
 Na+ reabsorption


65% is reabsorbed in the proximal tubules
25% is reclaimed in the Loops of Henle
 Aldosterone  active reabsorption of remaining Na+ in
DCT and collecting ducts
 Water follows Na+
Aldosterone
 Renin-angiotensin mechanism is the main trigger for
aldosterone release
 Specialized cells of JGA secrete renin in response to



Sympathetic nervous system stimulation
 Filtrate osmolality (decreased sodium)
 Stretch (due to  blood pressure)
Efferent
arteriole
Glomerular capsule
Glomerulus
Afferent
arteriole
Parietal layer
of glomerular
capsule
Capsular
space
Foot processes
of podocytes
Podocyte cell
body (visceral
layer)
Red blood cell
Proximal
tubule cell
Efferent
arteriole
Juxtaglomerular
apparatus
• Macula densa cells
of the ascending limb
of loop of Henle
• Extraglomerular
mesangial cells
• Granular cells
Afferent arteriole
Juxtaglomerular
apparatus
Lumens of
glomerular
capillaries
Endothelial cell
of glomerular
capillary
Mesangial cells
between capillaries
Renal corpuscle
Figure 25.8
Aldosterone
 Renin catalyzes the production of angiotensin II
 Prompts aldosterone release from the adrenal cortex


Targets cells of DCT and collecting ducts
Initiates sodium reabsorption
 Causes systemic vasoconstriction
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
Systemic
blood pressure/volume
Filtrate NaCl concentration in
ascending limb of loop of Henle
Stretch in afferent
arterioles
(+)
Inhibits baroreceptors
in blood vessels
(+)
(+)
(+)
Granular cells of kidneys
Sympathetic
nervous system
Release
(+)
Renin
Systemic arterioles
Causes
Catalyzes conversion
Angiotensinogen
(from liver)
Angiotensin I
Vasoconstriction
Results in
Converting enzyme (in lungs)
(+)
Peripheral resistance
Angiotensin II
Posterior pituitary
(+)
(+)
Releases
(+)
Systemic arterioles
Causes
Vasoconstriction
Results in
Peripheral resistance
Adrenal cortex
ADH (antidiuretic
hormone)
Secretes
(+)
Aldosterone
Targets
Collecting ducts
of kidneys
Causes
Distal kidney tubules
Causes
H2O reabsorption
Na+ (and H2O)
reabsorption
Results in
Blood volume
(+) stimulates
Blood pressure
Renin-angiotensin system
Neural regulation (sympathetic
nervous system effects)
ADH release and effects
Figure 26.10
Renin-Angiotensin System
 Increases blood volume
 Vasoconstriction
Increase BP
Aldosterone produced in response to:
 Decreased blood volume
 Decreased BP
 Low plasma sodium
 High plasma potassium
Factors Affecting Urine Volume
 Increased temperature
 Increases vasodilation and perspiration
 Decreases blood flow to kidneys
 Decreased temperature
 Increases blood flow to kidneys
Diuretics
 Chemicals that increase urine output
 Osmotic diuretics

Substances not reabsorbed
 Glucose in a diabetic patient
 ADH inhibitors

Alcohol and water
 Substances that inhibit Na+ reabsorption

Caffeine, thiazides, loop inhibitors
 Potassium levels are affected by some diuretics
Factors Affecting Urine Output
 ↑ blood pressure
 ↑ blood solute concentration
 ↓ plasma proteins
 Psychological factors
 Anxious  increased frequency and urge
 Fright  decreases urine output volume
Activities
 Regulation of Sodium Balance Worksheet
 Urinary 26 – Complete 1, 2, 4, & 5
 Urinary 27 – Complete 2, 3, & 5
Show me completed worksheets