What four systemic factors stimulate the release of renin?
Decreased blood pressure
Decreased fluid volume
Decreased sodium level
Increased B1 sympathetic activity
What five systemic factors inhibit the release of renin?
Increased blood pressure
Increased fluid volume
Increased NAP (natriauretic peptide) hormone
Increased sodium level
Decreased B1 sympathetic activity
What is juxtagolmerular apparatus and what are its four components?
•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.
Up to how much can the kidneys concentrate urine?
1200 - 1400 mOsm/L
What is the minimum required volume of average urine output and its solute concentration?
Which hormone primary regulates whether the kidney excretes dilute or concentrated urine?
antidiuretic hormone (ADH)
Antidiuretic hormone alter the rate of renal excretion of the solutes.
It alters the rate of renal excretion of water.
Where is ADH produced and secreted?
ADH is synthesized in the hypothalamus
ADH is stored and released by the posterior pituitary gland
What two effects does antidiuretic hormone produce?
What two receptors are involved in causing the hypothalamus release the antidiuretic hormone?
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
What is another name for antidiuretic hormone?
State where the factors below will stimulate or inhibit the relase of antidiuretic hormone:
a. angiotensin II
d. decreased serum sodium
f. atrial natriuretic peptide hormone
a. angiotenin II: stimulate
b. alcohol: inhibit
c. nausea: stimulate
d. decrased serum sodium: inhibit
e. pain: stimulate
f. atrial natriuretic peptide hormone: inhibit
h. narcotics: stimulate
i. hypervolemia: inhibit
What three effects does the antidiuretic hormone have on the kidneys?
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
Name the tubules that are impermeable to water.
ascending limb of the loop of henle
distal convoluted tubule
What is the primary purpose of urea reabsorption?
It increases interstitum hypertonicity to reabsorb water.
How does macula densa contribute to the release of renin?
When the macula densa in the distal convoluted tubule senses low sodium excretion, it causes the juxtaglomerular cells to release renin.
What effects does angiotensin II cause?
Vasoconstriction (main) to increase blood pressure
Posterior pituitary gland releases ADH
Adrenal gland releases aldosterone
Increased sympathetic activity
Negative feedback of renin release
What does renin do once it enters the systemic circulation?
It converts angiotensinogen to angiotensin I
Where is angiotensinogen synthesized?
In the liver
What is the function of angiotensin-converting enzyme?
Where is it found?
It converts angiotensin I to angiotensin II.
It is found mainly in the liver but also found throughout the blood vessels.
What effect does angiotensin II have on the afferent and efferent arterioles?
How does angiotensin II maintain GFR?
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.
Where is aldosterone produced?
In the zona glomerulosa of the adrenal cortex in the adrenal gland
What is aldosterone and what stimulates its production and release?
It is a mineralocorticoid hormone of the adrenal gland.
-elevated serum potassium
-decreased serum sodium
What is the renal effect of aldosterone?
•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+
Describe the renin-angiotensin system (RAS)
What is Conn's syndrome?
–Aldosterone secreting tumor causes hypertension, hypernatremia, and hypokalemia
(Excessive reabsorption of Na+ and excretion of K+ in the renal system)
What are the four mechanisms for renal concentration and dilution?
•Antidiuretic hormone (ADH)
•Atrial natriuretic peptide (ANP)
•The countercurrent multiplier
•The role of urea
What is the osmolarity of the interstitium in the renal cortex?
What is the osmolarity of the proximal tubule and where is it located in the kidney.
in the cortex of the kidney
What type of nephron has the loop of henle extending down to the renal medulla?
In juxtamedullary nephrons, state which tubules are located in the cortex and which are in the medulla.
Proximal and distal convoluted tubules are situated in the cortex.
Loop of henle is situated in the medulla.
How does the interstitium osmolarity change from the renal cortex to renal medulla?
The osmolarity of the renal cortex interstitium is iso-osmotic. The osmolarity becomes more hypertonic with increased depth of the medullary interstitium.
Osmolarity: inner medulla > outer medulla > cortex
Describe the changes that occur in the descending tubule, its osmolarity, and fluid concentration.
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
Describe the changes that occur in the ascending tubule, its osmolarity, and fluid concentration.
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).
Where is the thick ascending loop located?
In the outer medulla portion of the loop of henle
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.
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
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
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
What are the two basic requirements for forming a concentrated urine?
(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
(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.
What is the osmolar tonicity of the medullary interstitium surrounding the collecting duct?
What is the osmolarity of the medullary interstitium surrounding the distal convoluted tubule?
How do reabsorbed water and solutes in the renal interstitium enter into the systemic circulation?
By vasa recta and peritubular capillaries
What is the process by which renal medullary interstitium becomes hyperosmotic?
countercurrent multiplier mechanism.
What is the complication of ammonia toxicity?
What is urea?
A byproduct of amino acid (protein) metabolism consisting of 2 ammonia molecules.
Approximately 25-30 g/ day are made in the liver
What converts ammonia into urea?
Which solutes play an important role in generating a hypertonic interstitium when the kidney is forming a maximally concentrated urine?
Urea contributes 40% of the osmolarity of renal medulla gradient during max urine concentration
Where is urea reabsorbed and how does it function to reabsorb water?
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.
What transport mechanism is responsible for urea reabsorption?
Urea is recirculated from medulla interstitium into loop of Henle and returned to tubular fluid
What special anatomical arrangement does the countercurrent multiplier mechanism depend on?
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.
Is urine normally hypotonic, isotonic, or hypertonic?
hypotonic d/t dilution of urine
The osmolarity of the fluid in the collecting duct can be as low as 50mOsm/L.
In the presence of ADH, is urine hypotonic, isotonic, or hypertonic?
The osmolarity of the fluid in the collecting duct can reach as high as 1200mOsm/L.
Describe the different interstitium osmolarity and tubular osmolarity without the presence of ADH.
Describe the different interstitium osmolarity and tubular osmolarity in the presence of ADH.
Which tubule plays a major role in sustaining a hyperosmotic characteristic of the interstitium and how?
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.
In which tubule does the tubular fluid osmolarity quickly become equal to the renal medullary osmolarity and how?
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.
When ADH is present, water is reabsorbed from which tubules?
Cortical collecting tubule (mostly) and medullary collecting duct (minimal).
What are the 2 functions of Vasa Recta?
–Remove reabsorbed fluid from the interstitium
–Minimize solute uptake from the medulla (maintains medullary hypertonicity)
Explain the countercurrent exchange in vasa recta.
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
Explain how vasa recta helps to preserve the hyperosmotic interstitium.
•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
Do the vasa recta create the medullary hyperosmolarity?
No, the vasa recta do not create the medullary hyperosmolarity,
but they do prevent it from being dissipated.
How do vasodilators affect the urine concentrating ability?
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.