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200 Cards in this Set

  • Front
  • Back
what is the percent of filtered water reabsorbed in the proximal tubule?
67% - more than other part of the nephron
what is the percent of filtered water reabsorbed in the thin descending limb of loop of henle?
13%
the distal tubule and collecting duct are only permeable to H2O when?
when AVP (ADH) is present (transcellular transport)
are the thin and thick ascending limbs of the loop of henle permeable to H2O?
no
what percent of the water is excreted?
<1%
what percent of the filtered water is reabsorbed in the distal convoluted tubule?
10%
what percent of the filtered water is reabsorbed in the collecting duct?
9%
the renal tubule is formed by what?
a single layer of epithelial cells
functions along the tubule vary b/c different segments have different what?
1. permeabilities
2. transcellular potential differences
3. transport mechanisms
when is K+ balance achieved?
when urinary excretion of K+ exactly equals intake of K+ in the diet
the distal tubule and collecting duct have what type of charge?
very negative - this helps w/ secretion
what type of charge does the thick ascending limb of the loop of henle have?
very positive - helps w/ reabsorption
what type of charge does the thick decending limb of the loop of henle have?
slightly negative - drives ions in
what type of charge does the proximal tubule have?
slightly positive - helps to drive ions out
nutrients like sugars and AAs along w/ other nutrients are reabsorbed by the what?
proximal tubule
about _____ of the total volume of filtrate is resorbed by the proximal tubule but nearly _____ of filtered AAs and glucose are rearbsorbed.
2/3 ; 100%
Interstitial fluid (ISF) = ?
Extracellular fluid (ECF) = ?
interstitial fluid is equal to the fluid in between the cell; extracellular fluid is equal to the ISF + plasma
1. in the proximal tubule, how are Glucose, AA, and other substances transported from the lumen into the proximal tubule cell?
2. how do Glucose, AAs, and other substances leave the proximal tubule cell and enter the ISF?
1. symport active transport w/ Na+
2. by passive transport
What are SGLT2 and SGLT1?
SGLT2 is a weak high volume symporter in the early proximal tubule and SGLT1 is a strong symporter in the later half of the proximal tubule
reabsorption of nutrients primarily occurs along what part of the proximal tubule?
first 1/2
secretion of organic acids and bases primarily occurs along what part of the proximal tubule?
2nd half
what is inulin?
a sugar not normally found in the body, the amount remains constant
is creatinine secreted?
slightly secreted in the last 1/3 of the proximal tubule
when the conc. of glucose w/i the proximal tubule exceed's it's transport max (amount that can be reabsorbed/min), what happens?
glucose is excreted in the urine
the max amount of glucose that can be reabsorbed is about what?
300 mg/ml ( look at pg. 40 in notes)
where does NaCl reabsorption occur?
all along the tubule and collecting duct - different transport mechanisms are used in the different segments
1. how is Na+ reabsorbed in the early proximal tubule?
2. late proximal tubule?
1. - symport w/ nutrients
- antiport w/ H+
2. - transported w/ Cl-
- paracellular movement of NaCl
(leaves proximal tubule to enter ISF through symport transport w/ HCO3- and primary active transport w/ K+; Cl- passively exits the late proximal tubule to the ISF)
how is Na+ reabsorbed in the thick ascending loop?
- 1Na/2Cl/K cotransport
- Na/H antiporter
how is Na+ reabsorbed in the distal tubule?
Na/Cl symporter (it leaves the early distal tubule to enter the ISF through primary active transport w/ K+, Cl- enters ISF through channels)
how is Na+ reabsorbed in the late distal tubule and collecting duct?
Na+ channels controlled by aldosterone - leaves by primary active transport w/ K+
distinguish the difference in the roles of ADH and aldosterone
aldosterone controlls Na+ and K+ channels, ADH controls aquaporins and regulates H2O reabsorption
1. How is Na+ reabsorbed in the loop of Henle (TAL)?
2. How does it leave TAL and enter the ISF?
1. - w/ 2 Cl- and K+
- exchanged for H+
2. primary active transport (3Na+ leave and 2K+ enter), Cl- leaves through channels
how does water move through membranes?
passively, down an osmotic gradient
how does H2O move transcellularly and paracellularly?
transcellularly through aquaporins and paracellularly through leaky junctions
arginine vasopressin (AVP) controls what in the late distal tubule and collecting duct?
the # of apical membrane aquaporines
where does paracellular transport occur in the nephron?
proximal tubule and desceding loop of henle
what is the most important buffer in the ECF?
HCO3-
how is HCO3- destroyed?
continually destroyed in ECF by:
- buffering of metabolic acids
- filtration into the renal filtrate
1. what is responsible for making HCO3- to replace what is destroyed?
2. explain the process
1. the kidney
2.- tubular cells make H2CO3 which ionizes to form H+ and HCO3-
- HCO3- is reabsorbed into the ECF
- H+ is secreted into the filtrate
- to prevent the filtrate from becoming too acidic, the secreted H+ must be buffered
H+ secreted into the filtrate are buffered by what?
1. filtered HCO3-
2. filtered phosphates
3. other buffers (sulfates, creatinine)
secretion of what else is also very important in the synthesis of HCO3-?
NH4+
differentiate between what happens to a substance if it is released into the lumen of the tubule and the ISF surrounding the tubule?
if it is released into the lumen it is secreted, if it is released into the ISF it is reabsorbed
what does carbonic anhydrase (CA) do in the lumen and in the proximal tubule?
- in the lumen HCO3- combines w/ H+ to form H2CO3, CA then converts H2CO3 to H2O and CO2
- in the proximal tubule CA converts CO2 and H2O to H2CO3, H2CO3 then dissociates to form H+ and HCO3-, H+ is secreted into the lumen and HCO3- is rearbsorbed into the ISF
the secretion of H+ and the reabsorption of HCO3- is upregulated by what and down regulated by what?
upregulated by high CO2 (acidosis) and down regulated by alkalosis
when is the phosphate buffer a much better buffer?
due to its pK, it is a much better buffer as the pH of the filtrate becomes more acidic in the collecting duct
how does a phosphate buffer act?
it is filtered into the lumen as Na+HPO4-2 and combines w/ H+ to form Na+H2PO4- which is excreted
where are H+ and HCO3- made in the late distal tubule and cortical collecting duct?
intercalated cells:
- alpha intercalated cells secrete hydrogen ions and reabsorb bicarbonate ions (when plasma pH is low)
- beta intercalated cells secrete bicarbonate ions and reabsorb hydrogen ions (when plasma pH is high)
what do alpha cells do?
secrete hydrogen ions into the lumen and add bicarbonate to the ECF. these are strong H+ pumps that can acidify the urine down to a pH of about 4.5 - help to raise the plasma pH
what do beta cells do?
secrete HCO3- and add H+ to the ECF - help lower the plasma pH
what hormone increases renal H+ secretion?
aldosterone
for every NH4+ excreted, one new ______ enters the blood
HCO3-
in which tubule is NH4+ synthesized?
proximal tubule mostly
what is NH4+ synthesized from?
glutamine (from liver) is broken down to 2NH4+, 2HCO3-, and 1/2 a glucose
1. what percent of amino groups are excreted by the kidneys as urea?
2. what percent of amino groups are converted to glutamine?
1. 95%; 50% of this group starts out as NH4+ which produces 1 H+ in its conversion to urea and the other 1/2 start out as aspartate which produces 1 HCO3- in its conversion to urea
2. 5%; NH4+ combines w/ glutamate to form glutamine which travels in the blood to the kidney
from 1 glutamine what is excreted and what is absorbed?
2 NH4+ are excreted and 2 HCO3- are absorbed (rate increases w/ acidosis)
from 1 glutamine what is excreted and what is absorbed?
2 NH4+ are excreted and 2 HCO3- are absorbed (rate increases w/ acidosis)
why does ammonia enter the medulla ISF?
most bypass the distal tubule to prevent reabsorption from distal tubule and re-enter into the collecting duct to be excreted
what percent of new HCO3- formed involves NH4 formation?
60%, the other 40% involves titrable buffers like phosphates
what happens to the pH as you move from the proximal tubule to the collecting duct?
it decreases - it is 6.8 in the proximal tubule, 6.0 in the thick loop, and 4.4 by the time you get to the end of the collecting duct (lose buffering action)
compare how much new and filtered HCO3- is found in the proximal tubule through the collecting duct to excretion
1. proximal = 80% F 78% N
2. thick loop = 10% F 0% N
3. distal = 6% F 7% N
4. collecting = 4% F 15% N
5. exretion = 0% of either
normal plasma bicarbonate is about what?
24 meq/L
1. what happens when the plasma [HCO3-] increases above normal?
2. what happens when the plasma [HCO3-] decreases below normal?
1. the excess HCO3- is excreted and less is formed by the tubular cell
2. all of the filtered HCO3- is replaced and the tubular cells increase new HCO3- formation
what effect on H+ secretion and HCO3- reabsorption does increased PCO2 or decreased ECF pH have?
they both increase H+ secretion and HCO3- reabsorption
what effect does increased ECF K+ have on H+ secretion and HCO3- reabsorption?
it decreases H+ secretion and HCO3- reabsorption
what effect do increased aldosterone or glucocorticoids have on H+ secretion and HCO3- reabsorption?
increases them both
how is plasma pH controlled?
1. lungs - controls plasma [CO2]
2. kidneys - control plasma [HCO3-]
what are the 4 respiratory pH problems?
1. acute respiratory acidosis - renal compensation has not yet occured
2. chronic respiratory acidosis - renal compensation has occured
3. acute respiratory alkalosis - renal compensation has not yet occured
4. chronic respiratory alkalosis - renal compensation has occured
Metabolic acidosis
1. primary disturbance
2. compensation
1. decreased [HCO3-]
2. decreased PCO2 through hyperventilation (respiratory compensation)
metabolic alkalosis
1. primary disturbance
2. compensation
1. increased [HCO3-]
2. increased PCO2 through hypoventilation (respiratory compensation)
respiratory alkalosis
1. primary disturbance
2. compensation
1. lowered PCO2
2. lower [HCO3-] reabsorption and decrease H+ excretion (renal compensation)
respiratory acidosis
1. primary disturbance
2. compensation
1. increased PCO2
2. increased [HCO3-] reabsorption and increased H+ excretion (renal compensation)
name 4 metabolic pH problems
1. acute metabolic acidosis - respiratory compensation has not yet occurred
2. chronic metabolic acidosis - respiratory compensation has occurred
3. acute metabolic alkalosis - respiratory compensation has not yet occured
4. chronic metabolic acidosis - respiratory compensation has occurred
what is the normal plasma pH range?
7.38-7.44
what is the normal PCO2 range in the plasma?
33 - 42
what is the normal HCO3 range in the plasma?
22-28
1. what causes respiratory acidosis?
2. what causes respiratory alkalosis?
1. hypoventilation
2. hyperventilation
1. what causes metabolic acidosis?
2. what causes metabolic alkalosis?
1. exercise and acidic food
2. basic food
1. how do the kidneys compensate for respiratory acidosis and alkalosis?
2. what initiates this compensation by the kidneys?
1. by making more or less HCO3-
2. effect on enzymes by pH
are Ca++, Mg++, and Pi controlled together or separately? why?
together b/c:
1. the majority of these ions are in bone
2. many of these ions when in the plasma are bound to plasma proteins in inorganic anions
3. only free (or complexed w/ small anions) Ca++, Mg++, and Pi ions are filtered
4. parathyroid hormone (PTH) along w/ dietary intake and vit. D, control the free ion plasma concentrations
how much calcium is reabsorbed in the:
1. proximal tubule
2. thick ascending loop
3. distal tubule
4. collecting duct
1. 65% - mostly by paracellular transport which is passive and cannot be controlled
2. 25% - 50% by paracellular and 50% by transcellular (transcellular stimulated by PTH and D3)
3. 8% - 50% by paracellular and 50% by transcellular (transcellular stimulated by PTH and D3)
4. 1%
what percentage of the Ca++ is excreted in the urine?
1%
how much Pi is reabsorbed by the:
1. proximal tubule
2. thick ascending loop
3. distal tubule
4. collecting duct
1. 80% - inhibited by PTH
2. <1%
3. 10%
3. <1%
how much Pi is excreted in urine?
10%
how much Mg++ is reabsorbed by the:
1. proximal tubule
2. thick ascending loop
3. distal tubule
4. collecting duct
1. 15% - transcellular, stimulated by PTH
2. 70% - transcellular (stimulated by PTH) and paracellular
3 and 4. 10%
how much Mg++ is excreted in the urine?
5%
the transcellular transport of Mg2+ and Ca2+ are affected by what?
changes in concentration and electrical gradients
where is vit. D formed?
starts in skin, liver puts on 25 group, and the kidney puts on the 1 making 1, 25D3 which is the active form allowing the intestine to absorb Ca++ and Pi
if Ca++ decreases in the ISF what hormone increases?
PTH
what effect does PTH have on Mg++, Ca++, and Pi reabsorption?
PTH causes production of cAMP and PLC which stimulates the reabsorption of Mg2+ (in proximal tubule) and Ca++ (in thick ascending loop and distal tubule) and inhibits contransport of Pi w/ Na+ (in proximal tubule)
what do PLC and Pi do to vit. D?
they cause 25D3 to be converted to 1,25D3 (the active form) so it can cause absorption of Ca++ and PI in the intestine
what happens if the filtered proteins or peptides increase much over normal?
some will be excreted
small filtered proteins and peptides are reabsorbed by what 3 processes in the proximal tubule?
1. oligopeptides (n=2 to 4) are cotransported w/ H+
2. most peptides are digested by brush border peptidases and reabsorbed as AAs
3. small filtered proteins undergo endocytosis, digested by lysosomal enzymes, and returned to the blood as AAs
1. what does hypokalemia do to cells of the body?
2. what does hyperkalemia do to cells of the body?
1. hyperpolarizes cells of the body (including cardiac myocytes)
2. hypopolarizes cells of the body (including cardiac myocytes)
hypokalemia or hyperkalemia can cause what in the heart?
cardiac arrest and arrythmias
how is the resting membrane potential created?
mostly by K+ leaking out down it's concentration gradient
how is the resting membrane changed when extracellular [K+] changes?
the gradient changes
1. increased plasma [K+] = ?
2. decreased plasma [K+] = ?
1. hypopolarized
2. hyperpolarized
is most K+ extracellular or intracellular?
intracellular (98%)
dietary K+ changes while ECF [K+] _______
remain rather constant
what 3 processes keep ECF [K+] rather constant?
1. shifting of K+ in and out of cells (fast)
2. renal excretion of excess K+ (slow)
3. renal reabsorption of K+ when ECF [K+] is low
our diet causes ECF [K+] to increase which stimulates what?
an increase in epinephrine, insulin, and aldosterone which causes K+ to be actively pumped into the body cells (3Na+ out for 2K+ in). increased ECF [K+] also stimulates K+ to be exchanged for H+ inside the body cells
alkalosis (decreased osmolarity) has what effect on the K+/H+ exchange?
it stimulates the exchange and promotes the release of H+ from the body cells and the uptake of K+ by the body cells
what effect does acidosis (?osmolarity) have on the K+/H+ exchange?
it inhibits it
1. most filtered K+ is reabsorbed by the what?
2. ECF K+ is primarily regulated by controlling what?
1. proximal tubule and thick ascending tubule (some K+ is also reabsorbed by the thick loop)
2. secretion of K+ (sometimes reabsorption) into the distal tubule and collecting duct
1. is K+ reabsorbed passively or actively in the proximal and distal tubule?
passively in the proximal tubule; active in the distal tubule
how is K+ moved in the distal tubule and collecting duct?
usually secreted; controlled by regulating the K+ channels through aldosterone
why does K+ not move paracellularly in the distal tubule and collecting duct?
b/c they have tight junctions
why is there a greater secretion of K+ in the late distal tubule and collecting duct?
1. large conc. gradient
2. large electrical gradient
how does the % of K reabsorption compare to eachother in the proximal tubule during hypokalemia, hyperkalemia, and normal states?
it remains constant - 67%
how does the % of K reabsorption compare to eachother in the thick loop during hypokalemia, hyperkalemia, and normal states?
it remains constant - 20%
compare the amount of K+ that is secreted or reabsorbed in the distal tubule during hypokalemia, normal state, and hyperkalemia?
1. hypokalemia - 3% R
2. normal - 10% S
3. hyperkalemia - 50% S
compare the amount of K+ that is secreted or reabsorbed in the collecting duct during hypokalemia, normal state, and hyperkalemia?
1. hypokalemia - 9% R
2. normal - 5% S
3. hyperkalemia - 30% S
reabsorption of K+ occurs in the distal tubule and collecting ducts during states of hypokalemia by the what?
active transporters in alpha intercalated cells (H+ is secreted and K+ is reabsorbed)
what are some things that increase K+ secretion?
1. increased ECF K+
2. increased rate of tubular flow (increased GFR)
3. increase in aldosterone (there is also a decrease in ECF K+)
4. increased neg. tubular charge (pulls K+ out into filtrate)
what effect does acidosis and increased H+ secretion have on K+ secretion?
it decreases it b/c H+ is competing w/ K+
increased K+ secretion decreases H+ secretion causing what?
increased [H+] in the ECF (acidosis)
why does increased tubular flow increase K+ secretion?
it washes out the secreted K+ which increases the K+ gradient leading to increased K+ secretion
what channels compete in the distal tubule and collecting duct?
(all on lumen side)
1. passive K+ channel
2. primary active exchange channels w/ H+
3. primary active H+ channel
4. passive Cl- channel leading to inside tubule cells
increased excretion of large anions and delivery of NaCl to the distal tubule and collecting duct causes what?
increases tubular charge and causes an increase in K+ secretion (increased neg. charge in lumen increases the electrical gradient)
the last 1/3 of the proximal tubule has a variety of transporters (mostly antiporters and symporters) that do what?
secrete organic acids and bases
organic anions and cations are are weak acids and bases meaning they ionize how?
only partially ionize - pH of solution affects their degree of ionization
after secretion, the pH of the filtrate will have what affect on the organic acids and bases?
will affect the ionization and passive reabsorption of the organic acids and bases
a more acidic filtrate increases excretion of what?
a more basic filtrate increases excretion of what?
1. weak bases
2. weak acids
if there is too much acid it will be secreted into the proximal tubule, why does it get trapped and excreted?
b/c the filtrate in the proximal tubule has a higher pH and the acid dissociates becoming ionized and trapped inside b/c it is lipid insoluble
adult males and females are approximately what % water?
males - 60% H2O
females - 50% H2O (b/c of a little more fat)
acute body weight changes usually indicate changes in what?
body water content (retaining more Na+ - salt)
what 2 mechanisms is body water regulated by?
1. water intake (thirst)
2. changes in renal reabsorption and excretion of water
what is the water input from:
1. drinks
2. food
3. oxidation
1. 1000 ml
2. 1200 ml
3. 300 ml
(2500 ml total)
what is the output of water in the:
1. skin and lungs
2. feces
3. kidneys (urine)
1. 900 ml
2. 100 ml
3. 1500 ml
(2500 ml total)
what is highly regulated to maintain normal osmolarity of the body?
only thirst and renal reabsorption
during heavy exercise, water loss through the skin can increase to what?
several L/hr
intracellular volume (ICV) and ECV make up what fraction of the fluid of the body?
ICV = 2/3
ECV = 1/3
how is plasma volume different from ISF?
similar but has more proteins
1. is the K+ free ion concentration greater in the ICF or the ECF?
2. Na+?
3. Cl-?
4. protein ?
1. K+ greater in ICF
2. Na+ greater in ISF
3. Cl- is greater in the ISF
4. protein is greater in ICF
(HCO3- and Ca+ are about equal and ICF contains organic phosphates while the ISF does not)
what is the composition of body fluids (plasma)?
-a lot of Na+
-a little K+
-little Ca+
-a lot of Cl-
-fair amount of proteins
-fair amount of HCO3-
what does the anion gap estimate?
the anions in the plasma not measured during standard blood analysis
what is the normal anion gap?
8-12 MEq/L which is mostly due to neg. charged plasma proteins
an increased anion gap is often due to what?
metabolic acidosis
in the ECF the major pos. ionis what? and the major neg. ions are what?
pos. = Na+
neg. = Cl- and HCO3-
how do you determine the anion gap (equation)?
you know:
pos. ions in plasma = neg. ions
therefore:
[Na+] = [Cl-] + [HCO3-] + [Anion Gap Ions-]
So:
anion gap= [Na+] - [Cl-] - [HCO3-]
how is osmolarity determined?
by the conc. of impermeable particles in a solution not by the total mass of solutes
normal body fluid osmolarity is about what?
285 mOsm/kg
an osmotic pressure difference of 1 mOsm/kg is equivalent to what?
a hydrostatic pressure of 20 mmHg
normal oncotic pressure is about what?
25 mmHg
increased ECF = increased # of _____
particles
vol. of any fluid compartment is regulated by what?
increasing or decreasig the # of particles w/i the compartment
higher conc. of impermeable particles inside a membrane creates what?
an osmotic gradient causing H2O to move into the compartment until the conc. of particles is equal on both sides of the membrane
what are osmotically active substances?
substances that remain w/i a compartment creating an osmotic gradient
compared to the normal osmolarity of body fluids, solutions may be
1. isotonic
2. hypertonic
3. hypotonic
1. same
2. greater
3. less
what are non-osmotically active substances?
substances permeable to cell membranes that enter all compartments so that they do not produce a gradient (don't stimulate osmotic receptors)
examples: urea, glycerol
what are 6 disturbances of volume and osmolarity?
1. hypotonic expansion (increased H2O)
2. isotonic expansion (increased H2O and NaCl)
3. hypertonic expansion (increased NaCl)
4. hypotonic contraction (loss of NaCl)
5. isotonic contraction (loss of NaCl and H2O)
6. hypertonic contraction (loss of H2O)
Na+ regulates fluid _____ and H2O regulates fluid _____
vol.; osmolarity
and increase in vol. = an increase in ______
pressure
ECF volume is primarily regulated by what?
renal reabsorption of NaCl (measure ECF w/ NaCl)
osmolarity of body fluids is primarily regulated by what?
renal reabsorption of H2O and thirst regulation of water intake
where are the osmoreceptors?
in the hypothalamus (cause release of ADH)
Na+ regulates fluid _____ and H2O regulates fluid _____
vol.; osmolarity
and increase in vol. = an increase in ______
pressure
ECF volume is primarily regulated by what?
renal reabsorption of NaCl (measure ECF w/ NaCl)
osmolarity of body fluids is primarily regulated by what?
renal reabsorption of H2O and thirst regulation of water intake
where are the osmoreceptors?
in the hypothalamus (cause release of ADH)
hyponatremia
too much water = NaCl diluted
hypernatremia
too little water = NaCl concentrated
ECF vol. increase results in what?
edema (abnormal heart) or hypertension (normal heart), caused by too much sodium
hypotension
ECF volum depletion, caused by too little sodium
stretch receptors
in walls of carotid and aortic sinuses , left atrium, intrathoracic veins, and renal arteries - measures blood pressure
if the stretch receptors measure blood pressure, how do they measure effective blood volume?
b/c of the direct relationship between blood pressure and blood volume
effective arterial blood volume
blood volume that normally allows the circulatory system to produce a normal blood pressure
decreased blood pressure in the carotid and aortic sinuses stimulates what type of activity?
sympathetic activity which has renal and systemic effects
high blood pressure stimulates receptors in the left atrium which results in what?
ANP release which increases filtration rate
if the pressure receptors in the kidney sense low blood volume, what do they do?
1. release renin which converts angiotensinogen to angiotensin I
2. stimulate the brain to release ADH (causing water reabsorption) and increase thirst
blood pressure to the kidney directly affects ______ reabsorption?
Na+
how is ECF volume measured?
by measuring blood pressure w/ pressure receptors
pressure receptors make changes to adjust the pressure in what ways?
1. renin-angiotensin II - aldosterone system
2. sympathetic n. activity to the kidney
3. atrial natriuretic peptide
4. arginine vasopressin (non-osmotic control)
1. how do you quickly increase blood pressure?
2. how do you slowly increase blood pressure?
3. how do you increase blood pressure in an emergency?
1. blood vessels - vasoconstriction
2. adrenal cortex release aldosterone which causes the kidneys to reabsorb NaCl
3. low effective arterial blood volume stimualtes pressure receptors which stimulates the brain to release ADH causing the kidney to reabsorb water and increase thirst
the sympathetic system regulates effective blood volume by doing what?
1. directly increasing vascular resistance
2. increasing renin-angiotensin I - angiotensin II - aldosterone
3. directly increasing tubular reabsorption of Na+
how does the sympathetic system:
1. reduce vascular volume?
2. increase ECF volume?
1. by vascular constriction
2. by retaining Na+
atrial cells release ANP in response to _______
stretch (increased atrial BP)
how does ANP get rid of Na+?
by increasing RBF and GFR causing Na+ excretion and by inhibiting Na+ reabsorption by tubular cells
ANP decreases ______ volume
ECF
ADH is released from the ______ in response to _______
ADH is released from the posterior pituitary in response to increased osmotic pressure. ADH is also released w/ large decreases in effective blood volume (a 10% decrease in blood volume will cause ADH to help increase ECF volume. under these conditions body osmolarity can decrease below normal)
ADH increases water reabsorption by what tubules?
primarily the distal tubule and collecting duct, but also increases Na+ reabsorption by the thick ascending tubule of henle's loops
what wrong when you have congestive heart failure?
heart is failing - not pumping enough blood or producing enough pressure. receptors that measure blood pressure won't be stimulated so they'll increase blood volume which helps a little at first but ultimately produces edema - given diuretics to help relieve the swelling
increased renal blood pressure causes what?
1. increased GFR = increased tubular flow and Na+ excretion
2. increased RBF which causes:
- partial washout of medullary gradient and decreases Na+ reabsorption by thin descending loop
-decreases oncotic pressure in peritubular capillaries which decreases Na+ reabsorption
what things stimulate Na+ reabsorption?
1. sympathetic stimulation
2. angiotensin II
3. aldosterone
4. ADH
what inhibits Na+ reabsorption?
1. dopamine
2. ANP
3. urodilatin
NaCl reabsorption increases when ECF volume ______ and decreases when ECF volume is ________
decreases; high
what is the range of the kidney's ability for Na+ excretion?
10 meq/day to 1000 meq/day
plasma volume is affected by what 4 things?
1. ECV
2. plasma proteins
3. blood pressure
4. tissue pressure
estrogens and glucocorticoids increase ______ reabsorption?
NaCl
increased excretion of ________ decreases NaCl reabsorption
sulfates and phosphates
diuretics decrease ______ reabsorption
NaCl
cell volume is controlled by what?
1. transport processes that determine the conc. of impermeable particles inside the cell
2. synthesis of impermeable molecules inside the cell
causes of edema (increased ISF volume)
1. chronically decreased effective arterial blood volume
2. decreased plasma proteins - not eating enough to produce plasma proteins
3. increased capillary permeability - lose oncotic pressure (can be caused by histamine)
4. dilation of arterioles
5. decreased renal blood pressure - kidney acts as though you have no vol. and builds up Na+
6. lymph blockage
normal osmolarity of body fluids is what?
285 mOsm/kg
osmolarity is regulated by what?
thirst control and renal reabsorption of water
renal reabsorption is regulated primarily by what?
ADH hormone
increased osmolarity (1%) and decreased effective blood volume (10%) stimulates what?
osmoreceptors in the hypothalamus which causes the pituitary to release ADH. ADH increases the H2O permeability in the distal tubule and collecting duct
aquaporins are controlled by what in the late distal tubular and collecting duct cells?
AVP which is equal to ADH
what causes ADH to increase H2O reabsorption in the distal tubular and collecting duct cells?
it binds to a V2 receptor in the ISF which causes cAMP to be produced. cAMP makes aquaporins