chapter 29 renal lecture 3 Flashcards
to excrete excess water consumed..
it is necessary to dilute filtrate as it passes along tubule
after ingestion of excess water, the kidney does what
excretes excess water, but relative solute excretion concentration stays the same
Does osmolality in PCT change?
as fluid goes through PCT, solutes and water are reabsorbed in equal proportions=PCT filtrate isosmotic to plasma
in descending loop of henle, what happens to filtrate
water is reabsorbed and filtrate becomes hyper osmotic and becomes hypertonic (in equilibrium with interstitium)
what happens to tubular fluid in ascending LOH
tubular fluid is diluted in thick segment with Na, K and Cl reabsorbed. this part of LOH is impermeable to water (even with ADH) so tubular fluid becomes more dilute as it flows up ascending LOH into the early DCT, about 100 mOmos
What is the osmolality of filtrate entering the early DCT
hypo osmotic, about 1/3 of normal osmolarity so 100 mOsmos
In the absence of ADH, what happens to tubular fluid in DCT and collecting duct
tubular fluid is further diluted, additional reabsorption of Na Cl, and osmolarity further decreases to about 50 mOsmos
what is mechanism for forming dilute urine
continue to reabsorb solutes from DCT and no additional reabsorption of water, resulting in excretion of dilute urine
How is water lost in the body
breathing, feces, skin evaporation and perspiration, and kidney elimination
how do the kidneys form concentrated urine during times of decreased intake
kidneys continue to excrete solutes while increasing water reabsorption and decreasing the volume of urine formed
what is maximum urine concentrating ability in humans
1200 to 1400 mOsmos
What is maximum concentrating ability of kidneys?
600 mOsm/L of solute each day
If maximum concentrating ability of urine is 1200, than the minimal volume of urine 0.5L/day
urine specific gravity
measures osmolarity of urine is about 1.002 to 1.028 rising .001 for every 35 to 40 mOsmo increase
what are some requirements for excreting a concentrated urine
high ADH levels and hyper osmotic renal medulla
what does high ADH do
increases the permeability of the DCTand collecting ducts to water thereby allowing tubular reabsorption of water
what does a high osmolarity of the renal interstitial fluid do
provides osmotic gradient necessary for water reabsorption to occur in the presence of high levels of ADH involves countercurrent multiplier mechanism
what does counter current multiplication involve
arrangement of LOH and vasa rectae, specialized peritubular capillaries of nephron
what percentage of renal medulla contains juxtamedullary nephrons
25% that have LOH and vasae rectae that go deep in the medulla before returning to cortex with some LOH dipping to the tips of renal papillae that project from medulla to renal pelvis, and vase rectae parallel loops of henle
what is the osmolarity of interstitial fluid in the medulla of the kidney
1200 to 1400 in pelvic tip of medulla, due to large accumulate of solutes
what contributes to buildup of solutes in renal medulla
1) active transport of na and co transport of K, CL, and other ions out of the TAL into medullary interstitium
2) active transport of ions from the CD into medullary interstitial
3) facilitated diffusion of urea from the inner medullary collecting ducts to medullary interstitial
4) diffusion of only small amounts of water from medullary tubules into interstitium
what happens to osmolarity of tubular fluid as it diffuses from descending LOH to ascending
water diffuses out of descending limb into interstitial and the tubular fluid osmolarity gradually increases as it flows towards tip of LOH
In the presence of ADH, which parts of kidney that are not normally permeable to water become permeable
DCT, cortical collecting tubule, and inner medullary collecting duct
which areas of kidney participate in active transport of NACL
PCT, thick ascending LOH, DCT, CT, medullary CD
which areas of kidney are normally permeable to water
PCT, thin descending limb of LOH
is the ascending LOH permeable to water
no
in the presence of ADH, which part of the kidney that is not normally permeable to urea becomes permeable to urea
medullary collecting duct
what areas of kidney are normally permeable to urea
PCT, thin descending and ascending LOH
which areas of kidney are impermeable to urea
TAL, DCT, CD
counter current multiplication creation of hyper osmotic renal medullary interstitial steps
repeated reabsorption of NACL by thick ascending limb and continued inflow of new NACL from PCT into LOH multiplies solute concentration in medullary interstitium
What is role of DCT and CD in excreting concentrated urine
hypo osmolar urine from ascending LOH enters DCT, and Na is actively transported from tubular fluid to interstitium and tubular fluid becomes more dilute as it enters collecting duct. in absence of ADH the DCT and CD are impermeable to water, and solutes are continually reabsorbed from filtrate.
In presence of ADH, Collecting tubule becomes permeable to water and water is reabsorbed into cortex interstitium - where it is sequestered back into blood by peritubular capillaries
How is renal medulla interstium fluid hyperosmolarity preserved
large amounts of water reabsorption in presence of ADH in the cortex interstitum rather than medullary interstitium
what happens to collecting ducts in presence of ADH
collecting ducts become permeable to water so fluid at end of collecting ducts are essentially the same osmolarity as the interstitial fluid of the renal medulla, about 1200 mOsmos. By reabsorbing as much water as possible and excreting the same amount of solutes making concentrated urine
What happens to urea in the presence of ADH and water shortage in body
large amounts of urea passively reabsorbed from inner medullary collecting ducts into interstitium
what is mechanism for reabsorption of urea
water flows up ascending LOH into DCT and cortical collecting tubules, in the presence of ADH, water is reabsorbed and urea concentration increases in tubule as it is not permeable in this area. upon arriving to medullary collecting duct and water is continually reabsorbed, and urea transporters take urine from medullary collecting ducts to renal interstitial fluid, but results in high urea levels in tubular fluid. Malnutrition people lack ability to concentrate urine, high protein diets people have a higher concentrating ability of urine
3 determining factors of urea excretion
1)urea concentration in plasma
2)GFR
3)renal tubular reabsorption of urea
urea is recirculated in kidney several times before it is excreted. urea concentration in tubular fluid increases incrementally as it moves through tubular fluid
In the presence of reduced GFR how is urea excretion effected
it is still excreted normally
what happens to urea when there is excess water in body
urine flow rate increased, reduced levels of urea in medullary collecting ducts and medullary interstitium. because there is low ADH, there is decreased permeability of inner medullary collecting ducts to water and urea, and more urea is excreted in urine
what does counter current exchange in vasa rectae do
preserves hyperosmolarity of renal medulla by providing sluggish blood flow resulting in less solute loss (counter current exchanger)and sufficient blood flow to meet metabolic needs of medulla (as medullary BF metabolic needs are low)
how does blood enter and leave medulla
vasa rectae at boundary of cortex and medulla
blood concentration in vasa rectae arrives as hyper osmolar or hypoosmolar
hyperosmolar, 1200 in equilibrium with medullary interstitium, but as it travels back from medulla to cortex it becomes less concentrated as water moves from interstitial to vasa rectae
What does U shape of vasa rectae provide
minimizes loss of solute from interstitim carries away only water and solutes that is absorbed from medullary tubules, preserving high concentration of solutes established by counter current mechanism
what does increased medullary blood flow do to urine concentrating ability
reduces urine concentration ability, such as large increases in arterial BP, washing out hyper osmotic interstitium
what are two crucial components of urine concentrating ability
ADH and hyper osmolarity of renal medullary interstitial fluid
where is renin produced
Juxtaglomerular apparatus
what are 4 components of Juxtaglomerular apparatus
1) modified smooth muscle cells in afferent arteriole
2) modified smooth muscle cells in efferent arteriole
3) extraglomerular mesangial cells
4) macula dense cells in DCT
where are macula densa located
DCT, sense salt concentrations
what are 3 triggers for RAAS
low BP, SNS stimulation, macula dense sense low salt concentrations
Describe RAAS in presence of low BP
renin secreted from JXA
renin cleaves angiotensinogen from liver to angiotensin I
angiotensin I converted to angiotensin II in lungs
angiotensin II is most potent vasoconstrictor
what are 5 actions of angiotensin II
1) vasoconstriction and increased BP
2) increased aldosterone synthesis and release
3) increased ADH
4) increased thirst
5) feedback inhibition of renin release
Where does Angio II act upon
constricts afferent and efferent arterioles, releases PGE to maintain GFR
Where is aldosterone synthesized
steroid hormone in zona glomerulosa of adrenal cortex
what causes release of aldosterone name 3
increased K levels in ECF
Angio II
Decreased Na levels
what are actions of aldosterone
acts on distal tubule and collecting ducts to cause K secretion and H in exchange for NA
*get rid of K and H
describe Conn’s Syndrome
Aldosterone secreting tumors tha cause HTN, hypernatremia, hypokalemia. The increased NA concentration exceeds ability of DCT and CD to reabsorb NA, but K excretion=hypokalemia
Where is ADH stored and released
ADH is synthesized in hypothalamus, stored and released in posterior pituitary, plays a role in conserving water by concentrating urine
what is stimuli for ADH release
- osmoreceptors in hypothalamus sense increased osmolality
- mechanoreceptors in atria and aorta detect decreases in volume
- angio II, SNS, nausea, hypoxia, pain
- decreased blood volume, BP
- morphine, nicotine, cyclophosphamide
what causes decreased ADH
- decreased plasma osmolality
- increased blood volume
- increased blood pressure
- alcohol
- clonadine, haloperidol
where does ADH act on
distal tubule, medullary collecting ducts, cortical collecting tubule
what does ADH do to permeability of collecting system to water
increases permeability
what happens when ADH is absent
collecting system is impermeable to water leading to dilute urine
what effect does ADH have on urea permeability
ADH increases urea permeability in medullary collecting ducts
what causes ADH to work
driving force to move water out of tubules to the interstitium-hypertonic salty interstitium
what does the countercurrent multiplier U shape in LOH provide
U shape of LOH allows flow in opposite directions
what does differences in permeability of certain nephron segments provide in counter current multiplication
allows for flow in opposite directions
where does energy for counter current multiplier come from
ATP NA/K ATPase
urea is a byproduct of what
amino acid metabolism
what is the thick ascending loop of hence impermeable to
water and urea
when is inner medulla permeable to urea
only in presence of ADH, urea diffuses into inner medulla and is trapped here
is the thin ascending limb permeable to urea
yes, urea diffuses into the tubule and is recycled
what is the role of urea in max concentration urine
40% of osmolarity of renal medulla gradient during maximum urine concentration
in low water states, what happens with urea in medullary collecting duct
urea passively diffuses from medullary collecting duct during water deficits when ADH present, and urea is recirculated from medulla interstitial to LOH and returned to tubular fluid
urea moves back and forth between?
outer and inner medulla
what are two functions of vasa rectae
1) remove reabsorbed fluid from interstitium to circulation
2) minimize solute uptake from medulla-maintains medullary hypertonicity
how does medullary blood flow contribute to solute concentration during countercurrent exchange in vasa rectae
1) low blood flow-sluggish flow minimizes solute loss
2) U shape act as countercurrent exchangers to minimize solute washout, with little net diffusion of interstitial by U shaped vessels
what happens in descending vasa rectae
more fluid leaves than solute enters because of the rapid flow
what happens in ascending vasa rectae
decreasing hydrostatic pressure and increased osmolarity of blood
in the vasa rectae is more fluid reabsorbed or lost
more fluid is reabsorbed than lost
what does aldosterone stimulation cause
K secretion, Na reabsorption in exchange for H excretion
