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

Figure 25.16a

Loop of Henle

Osmolality

of interstitial fluid (mOsm)

Inner

medulla

Outer

medulla

Cortex Active transport

Passive transport

Water impermeable

Countercurrent multiplier

The long loops of Henle of the

juxtamedullary nephrons

create the medullary

osmotic gradient.

H2O

H2O

H2O

H2O

H2O

H2O

H2O

NaCI

NaCI

NaCI

NaCI

NaCI

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

Figure 25.17b

Active transport

Passive transport

Small volume of

concentrated urine

Cortex

NaCI

NaCI

NaCI Urea

Urea

H2O

H2O

H2O

H2O

H2O

H2O

H2O

Outer

medulla

Inner

medulla

(b) Maximal ADH

DCT

Descending limb

of loop of Henle

Collecting duct

H2O

H2O

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

Figure 25.17a

Active transport

Passive transport

(a) Absence of ADH Large volume

of dilute urine

Collecting duct

Cortex

NaCI

NaCI

NaCI

Urea

Outer

medulla

Inner

medulla

DCT

H2O

H2O

Descending limb

of loop of Henle

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

Figure 26.6

Osmolality

Na+ concentration

in plasma

Stimulates

Releases

Osmoreceptors

in hypothalamus

Negative

feedback

inhibits

Posterior pituitary

ADH

Inhibits

Stimulates

Baroreceptors

in atrium and

large vessels

Stimulates Plasma volume

BP (10–15%)

Antidiuretic

hormone (ADH)

Targets

Effects

Results in

Collecting ducts

of kidneys

Osmolality

Plasma volume

Water reabsorption

Scant urine

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

2. Brainstem respiratory centers

Acts within 1–3 minutes

3. Renal mechanisms

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)

Figure 25.8

Glomerulus

Glomerular capsule

Afferent arteriole

Efferent arteriole

Red blood cell

Podocyte cell body (visceral layer)

Foot processes of podocytes Parietal layer

of glomerular capsule

Proximal tubule cell

Lumens of glomerular capillaries

Endothelial cell of glomerular capillary

Efferent arteriole

• Macula densa cells

of the ascending limb of loop of Henle

• Granular cells

• Extraglomerular

mesangial cells

Afferent arteriole

Capsular space

Renal corpuscle Juxtaglomerular

apparatus

Mesangial cells between capillaries

Juxtaglomerular

apparatus

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

Figure 26.8

K+ (or Na+) concentration

in blood plasma*

Stimulates

Releases

Targets

Renin-angiotensin

mechanism

Negative

feedback

inhibits

Adrenal cortex

Kidney tubules

Aldosterone

Effects

Restores

Homeostatic plasma

levels of Na+ and K+

Na+ reabsorption K+ secretion

Figure 26.10

Stretch in afferent

arterioles

Angiotensinogen

(from liver)

Na+ (and H2O)

reabsorption

Granular cells of kidneys

Renin

Posterior pituitary

Systemic arterioles

Angiotensin I

Angiotensin II

Systemic arterioles

Vasoconstriction Aldosterone

Blood volume

Blood pressure

Distal kidney tubules

Adrenal cortex

Vasoconstriction

Peripheral resistance

(+)

(+)

(+)

(+)

Peripheral resistance

H2O reabsorption

Inhibits baroreceptors

in blood vessels

Sympathetic

nervous system

ADH (antidiuretic

hormone)

Collecting ducts

of kidneys

Filtrate NaCl concentration in

ascending limb of loop of Henle

Causes

Causes

Causes

Causes

Results in

Secretes

Results in

Targets

Results in

Releases

Release

Catalyzes conversion

Converting enzyme (in lungs)

(+)

(+) (+)

(+)

(+)

(+)

(+) stimulates

Renin-angiotensin system

Neural regulation (sympathetic

nervous system effects)

ADH release and effects

Systemic

blood pressure/volume

Renin-Angiotensin System Increases blood volume

Vasoconstriction

Aldosterone produced in response to:

Decreased blood volume

Decreased BP

Low plasma sodium

High plasma potassium

Increase BP

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

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