Urine Concentration and Dilution; Regulation of Extracellular Fluid Osmolarity and Sodium Concentration

Question 1

What four systemic factors stimulate the release of renin?

Answer 1

Decreased blood pressure

Decreased fluid volume

Decreased sodium level

Increased B1 sympathetic activity

Question 2

What five systemic factors inhibit the release of renin?

Answer 2

Increased blood pressure

Increased fluid volume

Increased NAP (natriauretic peptide) hormone

Increased sodium level

Decreased B1 sympathetic activity

Question 3

What is juxtagolmerular apparatus and what are its four components?

Answer 3

• Site of renin synthesis
• The JGA consists of 4 components

–Afferent arteriole –Efferent arteriole –Extraglomerular mesangial cells–Macula densa cells in the distal tubule

***Above is per lecture powerpoint slides but it’s incorrect. The JGA consists of juxtaglomerular cells in the walls of the afferent and efferent arterioles and macula densa, both of which act to release renin. Macula densa can effect the constriction or dilation of afferent and efferent arterioles but neither of these capillaries contribute to renin release.

Question 4

Up to how much can the kidneys concentrate urine?

Answer 4

1200 - 1400 mOsm/L

Question 5

What is the minimum required volume of average urine output and its solute concentration?

Answer 5

0.5 liter

600mOsm/L

Question 6

Which hormone primary regulates whether the kidney excretes dilute or concentrated urine?

Answer 6

antidiuretic hormone (ADH)

Question 7

Antidiuretic hormone alter the rate of renal excretion of the solutes.

T/F

Answer 7

False.

It alters the rate of renal excretion of water.

Question 8

Where is ADH produced and secreted?

Answer 8

ADH is synthesized in the hypothalamus

ADH is stored and released by the posterior pituitary gland

Question 9

What two effects does antidiuretic hormone produce?

Answer 9

Water retention

vasoconstriction

Question 10

What two receptors are involved in causing the hypothalamus release the antidiuretic hormone?

Answer 10

Osmoreceptors in the hypothalamus in response to an increased serum osmolarity

Decreased blood pressure sensed by the baroreceptors of the carotid sinus and aortic arch

Question 11

What is another name for antidiuretic hormone?

Answer 11

Arginine vasopressin

Question 12

State where the factors below will stimulate or inhibit the relase of antidiuretic hormone:

a. angiotensin II
b. alcohol
c. nausea
d. decreased serum sodium
e. pain
f. atrial natriuretic peptide hormone
g. anesthesia
h. narcotics
i. hypervolemia

Answer 12

a. angiotenin II: stimulate
b. alcohol: inhibit
c. nausea: stimulate
d. decrased serum sodium: inhibit
e. pain: stimulate
f. atrial natriuretic peptide hormone: inhibit
g. anesthesia:stimulate
h. narcotics: stimulate
i. hypervolemia: inhibit

Question 13

What three effects does the antidiuretic hormone have on the kidneys?

Answer 13

1. Increases water permeability on the distal and collecting tubule to reabsorb water (main)
2. Increases sodium reabsorption in the loop of henle
3. Increases urea reabsorption

Question 14

Name the tubules that are impermeable to water.

Answer 14

ascending limb of the loop of henle

distal convoluted tubule

collecting duct.

Question 15

What is the primary purpose of urea reabsorption?

Answer 15

It increases interstitum hypertonicity to reabsorb water.

Question 16

How does macula densa contribute to the release of renin?

Answer 16

When the macula densa in the distal convoluted tubule senses low sodium excretion, it causes the juxtaglomerular cells to release renin.

Question 17

What effects does angiotensin II cause?

Answer 17

Vasoconstriction (main) to increase blood pressure

Posterior pituitary gland releases ADH

Adrenal gland releases aldosterone

Increased thirst

Increased sympathetic activity

Negative feedback of renin release

Question 18

What does renin do once it enters the systemic circulation?

Answer 18

It converts angiotensinogen to angiotensin I

Question 19

Where is angiotensinogen synthesized?

Answer 19

In the liver

Question 20

What is the function of angiotensin-converting enzyme?

Where is it found?

Answer 20

It converts angiotensin I to angiotensin II.

It is found mainly in the liver but also found throughout the blood vessels.

Question 21

What effect does angiotensin II have on the afferent and efferent arterioles?

How does angiotensin II maintain GFR?

Answer 21

Angiotensin II causes constriction of both the afferent and efferent arterioles.

It maintains GFR by causing the release of prostaglandins that dilate the afferent arteriole.

Question 22

Where is aldosterone produced?

Answer 22

In the zona glomerulosa of the adrenal cortex in the adrenal gland

Question 23

What is aldosterone and what stimulates its production and release?

Answer 23

It is a mineralocorticoid hormone of the adrenal gland.

Stimulation:

• elevated serum potassium
• angiotensin II
• decreased serum sodium

Question 24

What is the renal effect of aldosterone?

Answer 24

• Acts on distal tubule and collecting ducts to cause K+ secretion and also H+ in exchange for Na+
• Net effect is to retain Na+ and get rid of K+ and H+

Question 25

Describe the renin-angiotensin system (RAS)

Answer 25

Question 26

What is Conn’s syndrome?

Answer 26

Primary hyperaldosteronism.

–Aldosterone secreting tumor causes hypertension, hypernatremia, and hypokalemia

(Excessive reabsorption of Na+ and excretion of K+ in the renal system)

Question 27

What are the four mechanisms for renal concentration and dilution?

Answer 27

• Antidiuretic hormone (ADH)
• Atrial natriuretic peptide (ANP)
• The countercurrent multiplier
• The role of urea

Question 28

What is the osmolarity of the interstitium in the renal cortex?

Answer 28

280mOsm (iso-osmotic)

Question 29

What is the osmolarity of the proximal tubule and where is it located in the kidney.

Answer 29

280mOsm (iso-osmotic)

in the cortex of the kidney

Question 30

What type of nephron has the loop of henle extending down to the renal medulla?

Answer 30

juxtamedullary nephrons

Question 31

In juxtamedullary nephrons, state which tubules are located in the cortex and which are in the medulla.

Answer 31

Proximal and distal convoluted tubules are situated in the cortex.

Loop of henle is situated in the medulla.

Question 32

How does the interstitium osmolarity change from the renal cortex to renal medulla?

Answer 32

The osmolarity of the renal cortex interstitium is iso-osmotic. The osmolarity becomes more hypertonic with increased depth of the medullary interstitium.

cortex: iso-osmotic
medulla: hyper-osmotic

Osmolarity: inner medulla > outer medulla > cortex

Question 33

Describe the changes that occur in the descending tubule, its osmolarity, and fluid concentration.

Answer 33

As the tubule descend deeper into the renal medulla, the hyperosmolarity of the renal medulla interstitium causes osmosis of water from the tubule to the interstitium.

With the shift of the fluid out of the tubule, the tubular fluid becomes hyperosmotic (600mOsm/L) now equivalent to the hypertonicity of the medullary interstitium.

Osmolarity: begins as iso-osmotic but becomes hyperosmotic

Urine: concentrated.

Question 34

Describe the changes that occur in the ascending tubule, its osmolarity, and fluid concentration.

Answer 34

Na+, K+, Cl- are actively reabsorbed, especially in the thick ascending limb but water is not reaborbed (impermeable).

As the tubule continues to ascend, water becomes more diluted.

At the end of the ascending tubule, tubular fluid is hypo-osmotic (100mOsm/L) in relation to its interstitium (300mOsm/L).

Osmolarity: hypotonic

Fluid: diluted

Question 35

Where is the thick ascending loop located?

Answer 35

In the outer medulla portion of the loop of henle

Question 36

Describe the changes that occur in the distal convoluted tubule, cortical and medullary collect duct, and the osmolarity and fluid concentration in the three segments.

Answer 36

Normally in the absence of ADH, the three segments remain impermeable to water but contine to reabsorb Na+, Cl-, further decreasing its osmolarity and diluting urine.

Osmolarity: 100mOsm early distal tubule to 50mOsm in the collecting duct

Urine: diluted

Question 37

In healthy kidneys, fluid leaving the ascending
loop of Henle and early distal tubule is always dilute,
regardless of the level of ADH.

True / False

Answer 37

True

In the absence of ADH, the urine is further diluted in the late distal tubule and collecting ducts and a large volume of dilute urine is
excreted.

Question 38

What are the two basic requirements for forming a concentrated urine?

Answer 38

(1) a high level of ADH, which increases the permeability
of the distal tubules and collecting ducts to water,
thereby allowing these tubular segments to avidly reabsorb
water

(2) a high osmolarity of the renal medullary
interstitial fluid, which provides the osmotic gradient
necessary for water reabsorption to occur in the presence
of high levels of ADH.

Question 39

What is the osmolar tonicity of the medullary interstitium surrounding the collecting duct?

Answer 39

hyperosmotic

Question 40

What is the osmolarity of the medullary interstitium surrounding the distal convoluted tubule?

Answer 40

iso-osmotic (280mOsm/L)

Question 41

How do reabsorbed water and solutes in the renal interstitium enter into the systemic circulation?

Answer 41

By vasa recta and peritubular capillaries

Question 42

What is the process by which renal medullary interstitium becomes hyperosmotic?

Answer 42

countercurrent multiplier mechanism.

Question 43

What is the complication of ammonia toxicity?

Answer 43

encephalopathy

coma

death

Question 44

What is urea?

Answer 44

A byproduct of amino acid (protein) metabolism consisting of 2 ammonia molecules.

Approximately 25-30 g/ day are made in the liver

Question 45

What converts ammonia into urea?

Answer 45

The liver

Question 46

Which solutes play an important role in generating a hypertonic interstitium when the kidney is forming a maximally concentrated urine?

Answer 46

Urea

Urea contributes 40% of the osmolarity of renal medulla gradient during max urine concentration

Question 47

Where is urea reabsorbed and how does it function to reabsorb water?

Answer 47

Some urea is reabsorbed in the inner medulla by the thin ascending limb and most by the medullary collecting duct in the presence of ADH.

This creates a hypertonic interstitium to allow for better water reabsorption.

Urea is recirculated from medulla interstitium into loop of Henle and returned to tubular fluid and reabsorbed into the interstitium through the medullary collecting duct to further reabsorb water.

Question 48

What transport mechanism is responsible for urea reabsorption?

Answer 48

Facilitated diffusion

Urea is recirculated from medulla interstitium into loop of Henle and returned to tubular fluid

Question 49

What special anatomical arrangement does the countercurrent multiplier mechanism depend on?

Answer 49

The countercurrent multiplier mechanism depends on
the special anatomical arrangement of the loops of Henle
and the vasa recta, the specialized peritubular capillaries
of the renal medulla.

Question 50

Is urine normally hypotonic, isotonic, or hypertonic?

Answer 50

hypotonic d/t dilution of urine

The osmolarity of the fluid in the collecting duct can be as low as 50mOsm/L.

Question 51

In the presence of ADH, is urine hypotonic, isotonic, or hypertonic?

Answer 51

Hypertonic.

The osmolarity of the fluid in the collecting duct can reach as high as 1200mOsm/L.

Question 52

Describe the different interstitium osmolarity and tubular osmolarity without the presence of ADH.

Answer 52

Question 53

Describe the different interstitium osmolarity and tubular osmolarity in the presence of ADH.

Answer 53

Question 54

Which tubule plays a major role in sustaining a hyperosmotic characteristic of the interstitium and how?

Answer 54

A major reason for the high medullary osmolarity is active transport of sodium and co-transport of potassium, chloride, and other ions, such as urea, from the thick ascending loop of Henle into the interstitium.

The impermeability to water reabsorption further attributes to the hyperosmolarity of the interstitium.

Question 55

In which tubule does the tubular fluid osmolarity quickly become equal to the renal medullary osmolarity and how?

Answer 55

The descending limb of Henle’s loop, in contrast to
the ascending limb, is very permeable to water, and the
tubular fluid osmolarity quickly becomes equal to the
renal medullary osmolarity, as the limb loses water and becomes concentrated.

Question 56

When ADH is present, water is reabsorbed from which tubules?

Answer 56

Cortical collecting tubule (mostly) and medullary collecting duct (minimal).

Question 57

What are the 2 functions of Vasa Recta?

Answer 57

–Remove reabsorbed fluid from the interstitium

–Minimize solute uptake from the medulla (maintains medullary hypertonicity)

Question 58

Explain the countercurrent exchange in vasa recta.

Answer 58

Medullary blood flow contributes to solute concentration

1. Medullary blood flow is low

• 1-2% of total renal blood flow
• Sluggish flow minimizes solute loss (wash-out)

2. U-shaped Vasa recta

• Act as countercurrent exchangers to minimize solute washout
• Little net dilution of interstitium by U-shaped vessels

Question 59

Explain how vasa recta helps to preserve the hyperosmotic interstitium.

Answer 59

• In descending VR fluid leaves the VR because of the hydrostatic pressure and some solutes enter. More fluid leaves than solute enters.
• In the ascending VR the situation reverses because of the decreasing hydrostatic pressure and increasing osmolality of blood.
• Overall more fluid is reabsorbed than was lost

Question 60

Do the vasa recta create the medullary hyperosmolarity?

Answer 60

No, the vasa recta do not create the medullary hyperosmolarity,
but they do prevent it from being dissipated.

Question 61

How do vasodilators affect the urine concentrating ability?

Answer 61

Certain vasodilators can markedly increase renal medullary blood flow, thereby “washing out” some of the solutes from the renal medulla and reducing maximum urine-concentrating ability.