Lecture 18: Renal Phys Con't Flashcards
relate chronic HTN to the AA’s ability to autoregulate with dilation/constriction
chronic HTN > continuous constriction of AA to prevent overperfusion > harder to dilate in cases where pt becomes hypotensive
(3) causes of hardening/calcification of vasculature
- chronic HTN
- oxidative stress
- uncontrolled diabetes
describe what overperfusion would look like past the upper limits of autoregulation
- AA would attempt to constrict to prevent overperfusion (but would not be enough)
- GC pressure would increase leading to:
+increased NFP
+very fast filtration rate
+very fast reabsorption rate
+massive UOP
describe what underperfusion would look like past the lower limits of autoregulation
- the AA would attempt to dilate to prevent underperfusion (but wouldn’t be enough)
- GC pressure would decrease leading to:
+slower filtration rate
+slower reabsorption rate
+reduced UOP
describe how a slow fitration rate impacts reabsorption rate:
since there is more time spent in the tubule, there is a larger percentage of filtrate being reabsorbed by the PT caps
if filtration rate is slow, there’s not good filtration happening (more reabsorption)
beta blockers, beta agonists, CCBs, & pressors all affect this arteriole more
affects AA more
angiotensin affects this arteriole more
EA
since creatinine is freely filterable, as it travels further into the PCT, what would the [creatinine] be?
the [creat] would be more concentrated the further along it travels the PCT (d/t more water getting reabsorbed)
how much water gets reabsorbed at the PCT after filtration?
2/3
under normal circumstances, the macula densa “counts” a normal amount of these ions that pass by it
Na+
Cl-
under these conditions:
* higher filtration rate
* normal amount of reabsorption
the amount of NaCl at the TAL would be:
the MD would “count” MORE NaCl at the TAL d/t the high GFR
if the kidney filters MORE but does not reabsorb MORE, the MD cells would count MORE NaCl at the thick ascending limb
under these conditions:
* lower filtration rate
* normal amount of reabsorption
the amount of NaCl at the TAL would be:
the MD would count a LOW number of NaCl at the TAL d/t the LOW GFR
if the kidney filters LESS but does not reabsorb LESS, the MD cells would count LESS NaCl at the thick ascending limb and the MD cells would increase AT II levels to increase GFR
under these conditions:
* normal filtration rate
* increased Na+ and Cl- reabsorption at the PCT
the macula densa would sense the GFR to be?
the macula dense would sense the GFR to be LOW due to a less than normal amount of Na+ being counted at the TAL and AT II would be secreted leading to a HIGHER GFR
ACE-i’s, ARBs would prevent this
SGLT transporters in proximal tubule transports how many glucose per how many Na+?
1:1
1 glucose INTO cell for 1 Na+ INTO cell
Na+ travels down its concentration gradient pulling in 1 glucose molecule with it
secondary AT
INTO cell from TUBULE
a large increase in tubular glucose would have the following effects on reabsorption and GFR:
- increase in tubular glucose = increase in SGLT transportation of glucose AND sodium into cell
- increased Na+ into cell = more Na+ reabsorbed
- more Na+ reabsorbed means LESS Na+ at MACULA DENSA
- low Na+ count at MD = increase in AT II = increase in GFR
what is hyperfiltration?
- “wear & tear” on the nephrons causes accelerated loss of nephrons
chronic uncontrolled DM + amino acid intake
how many amino acids get transported with the Na+/AA transporter?
1:1
1 amino acid INTO cell for every 1 Na+ INTO the cell
secondary AT
a large increase in amino acids would have the following effects on reabsorption and GFR:
- increase in tubular amino acids = increase in Na+/AA transportation of amino acids AND sodium into cell
- increased Na+ into cell = more Na+ reabsorbed
- more Na+ reabsorbed means LESS Na+ at MACULA DENSA
- low Na+ count at MD = increase in AT II = increase in GFR
apical side of the cell =
tubular side of the cell wall
basolateral side of cell
interstitial fluid side of cell wall
list the basolateral transporters on a PCT cell:
- GLUT transporter (facilitated diffusion)
- Na+/K+/ATPase pump (primary AT)
list the apical co-transporters on a PCT cell:
- SGLT (secondary AT)
- Na+/AA (secondary AT)
list the basolateral antiporter on a PCT cell:
Na+/K+/ATPase pump
list the antiporter on the apical side of the PCT cell:
- NHE (sodium/hydrogen exchanger)
what is a PCT cell’s vrm?
-70 mV
this segment of the PCT reabsorbs 90% of the PCT’s glucose
S1 (SGLT-2 transporter)
this transporter transports 90% of the PCT glucose through the basolateral walls to the interstitum
GLUT-2
these segments of the PCT reabsorbs 10% of the PCT’s glucose
S2 & S3 segment (via SGLT-1 transporters)
these transporters transport 10% of the PCT’s glucose to the interstitium
GLUT-1
the SGLT-2 transporters cotransport how many Na+s and how many glucose?
- 1 Na+
- 1 glucose
the SGLT-1 transporters cotransport how many Na+s and how many glucose?
- 2 Na+
- 1 glucose
which SGLT transporter in the PCT has a higher affinity for Na+/glucose?
SGLT-1
explain why the SGLT-1 transporter has a higher affinity for Na+/glucose than the other SGLT transporter
SGLT-1 reabsorbs only about 10% of the glucose after SLGT-2 reabsorbs about 90% of glucose upstream; since the fluid that reaches segment 2 and 3 in the PCT is now very dilute, the SGLT-1 needs a much higher afinity to bind the remaining glucose (and sodium)
filtered load = ?
[compound being filtered] x qty of fluid being filtered per min
ex) 100 mg/dL of glucose x 1.25 dL plasma/min = 125 mg/min filtered load
at what plasma glucose [ ] does do the kidneys reach transport maximum?
about 300 mg/100 ml
around what plasma glucose [ ] does the kidney reach threshold
200 mg/100 ml
what does threshold mean in terms of glucose parmacokinetics?
it means that past 200 mg/100 ml of plasma glucose, more glucose will “sneak past” the initial segments of reabsorption to spill out into the urine
explain the primary pathway for AT II regulation on GFR:
- a drop in arterial pressure occurs
- decreased GCP
- decreased GFR
- decreased macula densa NaCl (d/t increased PCT reabsorption)
- increased renin release
- increased AT II release
- EA resistance increased
- increasing GCP
- increasing GFR
explain the secondary pathway for renal regulation of GFR:
- a drop in arterial pressure occurs
- decreased GCP
- decreased GFR
- decreased macula densa NaCl (d/t increased PCT reabsorption) > releases NITRIC OXIDE (NO)
- decreased AE resistance (increasing dilation)
- increasing GCP
- increasing GFR
if a drop in arterial pressure causes a decrease in RBF, how do the kidneys prevent a further reduction in RBF?
the AE simultaneously dilates alongside the EA constricting when AT II has been released; since the increase in EA resistance will cause a further drop in RBF, the AE counteracts that by dilating to prevent further reduction in RBF
which transporters do AT II speed up directly in the PCT?
- Na+/K+/ATPase
- NaHCO3 symporter
which transporter does AT II speed up indirectly in the PCT?
NHE
- the ICF [Na+] < ECF [Na+] and this gradient difference is caused by the Na+/K+/ATPase pump that is directly sped up by AT II
how does Cl- get reabsorbed in the PCT?
- it travels through paracellular routes, following Na+ bc of its positive charge
what is “bulk flow”?
bulk flow refers to:
* the sum of capillary forces leading to filtration in the GCs (10 mmHg)
* the sum of capillary forces leading to reabsorption in the PT caps (-10 mmHg)
what is urea and what is it’s role in osmosis?
- urea is a byproduct of metabolism and typically the body wants to get rid of it
- however, the kidneys keep urea around in the renal interstitium to help keep the renal intersitium concentrated to help reabsorb water via osmosis
paracellular pathway usually involves what kind of transport?
passive diffusion
transcellular pathway usually involves what type of transport?
active transport
what is the role of the brush border in the PCT?
- increases surface area for more transporters to be placed in the PCT
- increases surface area 20x fold
what side of the PCT cells would the brush/ border be found?
on the luminal side/apical side
Na+ travels through the cells via a ________ gradient
electro-chemical
* charge + [ ] gradient
what is the PCT’s tubular luminal net charge? which ion is typically responsible for this charge?
-3 mV - usually caused by leftover Cl- in the lumen
which ion does not usually build up it’s [ ] in the PCT?
Na+
Na+ usually gets reabsorbed at around the same rate water gets reabsorbed in the PCT
at what point in the proximal tubule does [Cl-] incease?
in the latter half of the proximal tubule; the further down the proximal tubule length, the more [Cl-] will be concentrated
what is endocytosis?
AKA pinocytosis
the PCT engulfs proteins in a vesicle and breaks them down into amino acids so that they can get reabsorbed into the PT capillaries
vesicles may come from brush border (?)
name (3) things that can go under endocytosis/pinocytosis in the PCT:
- albumin
- growth hormone
- peptides (10-20 amino acid string)
how much protein gets filtered daily?
1.8 g
how much protein gets reabsorbed daily?
1.7 g
how much protein usually gets excreted out through the urine daily?
100 mg
the NHE is a form of _____
secretion
the NHE actively secretes protons into the tubules
what reactions does carbonic anhydrase catalyze?
- CO2 + H2O to form carbonic acid (H2CO3)
- carbonic acid dissociation to H2O + CO2
carbonic anhydrase inhibitors cause what to occur in the PCT?
- slows down the NHE
- increases Na+/HCO3- concentrations in the lumen to cause mild diuresis
- causes metabolic acidosis (wasting of HCO3-)
where does production of new HCO3- usually occur?
PCT
what is the reaction that occurs for new HCO3- to be produced?
- glutamine (produced in the liver) travels into PCT cells
- 1 glutamine breaks down into: 2 HCO3- and 2 NH4+ (ammoniUM)
- the HCO3- gets reabsorbed via NaHCO3 pump
- 2 ammonium gets secreted via NH4+/Na+ antiporter
some extracellular buffers in the urine include:
- ammonium
- phosphate
- sodium phosphate
what ways can Ca2+ get reabsorbed in the PCT?
- primary AT Ca2+ pump (basolateral PMCA)
- NCX
can come into PCT cell via Ca2+ channel (along its gradient)
the amount of Ca2+ filtration that occurs depends on:
- how much albumin is present in the lumen
- how many other negatively charged proteins are present in the lumen
*Ca+ tends to aggregate with these proteins
which gland regulates Ca2+ levels?
parathyroid gland
with a decreased [Ca2+], how does the parathyroid respond?
- increased PTH leading to:
+increased vit D activation
+increased osteoCLAST activity
+decreased osteoBLAST activity
all of these processes lead to increased Ca2+ reabsorption
how does the parathyroid regulate intestinal Ca2+ reabsorption?
by increasing vitamin D activation; our dietary intake of vitamin D will get activated via parathyroid hormone
differentiate osteoclasts vs osteoblasts
- osteoclast - increase Ca2+ release (from Calcium-Phosphate bonds found in bone); osteoclasts break down bones
- osteoblast - increase bone building activity (increases Calcium-Phosphate bonding)
endogenous organic cation compound transporters transport the following:
- ACh
- choline
- creatinine
- dopa
- epi
- guanidine
- histamine
- 5HT
- NE
- thiamine
exogenous organic cation compound transporters transport the following:
- atropine
- isoproterenol
- morphine
- procaine
- quinine
- tetraethylammonium
endogenous organic anion compound transporters transport the following:
- bile salts
- fatty acids
- hippurates (PAH is not endogenous)
- oxalates
- PGGs
- urates
exogenous organic anion compound transporters transport the following:
- acetazolamide (diamox)
- cholorthiazide
- ethacrynate
- lasix
- PCN
- salicylates (ASA)
- sulfonamides
organic cations use this type of transporter:
H+ dependent ANTIPORTER
organic anions use this type of transporter:
Na+ dependent ANTIPORTERS
the further into the thin descending loop of henle, there is (more/less) solute concentration in the renal interstitium:
the deeper into the thin descending limb, the MORE solute concentration there is in the renal interstitium
* the thin descending loop is permeable to water
* the thin descending loop is fairly impermeable to ions
describe the thin ascending loop of henle in terms of permeability and transport:
- thin ascending loop is impermeable to H2O
- NaCl transporters (primary AT) reabsorb Na+ and Cl- here
+only reabsorbs small amounts of NaCl here
describe ion & water permeability in the thick ascending loop of henle (TAL)
- thick ascending is NOT permeable to water
- IS permeable to ions at this point
- reabsorbs CATIONIC electrolytes here (Na+ via transporters, and Mg2+/Ca2+ via paracellular routes)
- apical/luminal transporters include:
+NKCC2
+NHE
+K+ channel - basolateral/renal interstitium transporters include:
+Na+/K+/ATPase
+Cl- channels
+K+ channels
what is the net voltage in the TAL tubular lumen?
+8 mV
which diuretics work in the TAL and on what pump?
LOOP diuretics work in the THICK ASCENDING LOOP on the NKCC2 pump
name (3) loop diuretics listed in lecture:
- furosemide (lasix)
- ethacrynic acid
- bumetanide (bumex)
how does Mg+ and Ca2+ get reabsorbed in the TAL?
- the divalent molecules get reabsorbed via the paracellular route in the TAL
- this happens because K+ channels allow K+ to leak into the lumen, creating a more positively charged lumen (+8 mV)
- the positively charged lumen pushes the divalent molecules across the paracellular route
why are loop diuretics considered to be the “most powerful” diuretics?
- by inhibiting the NKCC2, the renal interstitium becomes less concentrated which means water is harder to reabsorb via osmosis
- more water ends up in the urine = increased UOP
what is the maximum osmolarity the renal interstitium can be?
1200 mOsm/L
what is the maximum osmolarity the kidneys can concentrate urine?
- 1200 mOsm/L
- this reflects that the kidneys are really trying to conserve water
if someone is given a loop diuretic, what might you expect their urine osmolarity to be?
< 1200 mOsm/L
this is because the renal interstitium will have a much lower osmolarity; therefore, the urine will also have to have a much lower osmolarity
where do thiazide diuretics work?
DCT
which transporters are found on the apical side of the DCT?
- NaCl symporter
- Ca2+ channels
which transporters are found on the basolateral side of the DCT?
- Na+/K+/ATPase pump
- primary AT Ca2+ pump
- NCX
which pump do thiazide diuretics inhibit?
NaCl pumps in the DCT
what stimulates apical Ca2+ channels in the DCT?
PTH
which molecules are principal cells sensitive to? where are they found?
- aldosterone
- found in DCT
which molecules are intercalated cells sensitive to? where are they found
- aldosterone
- ADH
- found in DCT
where are aldosterone receptors located?
INSIDE the cell
aldosterone is a cholesterol derivative and can easily cross the cell membrane
what are the effects of aldosterone agonism?
- speeds up the K+ channel diffusion out of the cell
- speeds up the Na+ diffusion into cell
- speeds up the Na+/K+/ATPase pump on the basolateral membrane of the cell wall
the metabolic rate of the PCT is:
high
about what percentage of water gets reabsorbed at the TDL after initially being filtered?
20%
PCT reabsorbs 2/3 of the water initially filtered
PCT + TDL percentage of water reabsorbed = ?
20% + 2/3(total water filtered) = 85% of water reabsorbed at the end of the TDL
the remaining percentage of water reabsorbed at late DCT/CD
15%
what percentage of ions get reabsorbed at the TAL?
25%
where are principal cells found?
the late portions of the DCT/all of the CD
what percentage of ions do the principal cells reabsorb/secrete?
100 x (2/3 of initially filtered ions at PCT) + 25% (at TAL) = ~91% total reabsorbed at this point, leaving 8% ions at DCT/CD AKA the remaining percentage
| 67 + 25 = 92; 100 - 92 = 8% remaining at DCT/CD
the TAL has a (low/high) metabolic rate?
high
what are the effects of thiazide diuretics on Ca2+?
- thiazide diuretics increase Ca2+ reabsorption
- Ca2+ reabsorption is increased by increasing the “spin” rate of the NCX (d/t lowering the ICF [Na+])
what other ways can thiazide diuretics be used in addition to being a diuretic?
- useful in pts with osteoporosis (increased Ca2+ reabsorption)
- useful in pts who are prone to kidney stones (decreases Ca2+ levels in the urine by increasing Ca2+ reabsorption)
what are 5 functions of aldosterone in principal cells?
- increases “spin” rate of Na+/K+/ATPase pump
- increases # of Na+ channels
- increases # of K+ channels
- increases Na+ reabsorption
- increaes K+ secretion
what is a ROMK channel
- renal outer medullary K+ channel
- these channels are usually sequestered in vesicles until needed to be utilized
- placed on the cell membrane in response to normal K+ excretion and open
- opens also in response to high K+ excretion situations
closed when the body is trying to conserve K+ (low K+ excretion)
what is a BK channel?
- “big potassium” channel
- remains closed under low K+ excretion conditions and normal K+ excretion conditions
- only opens up in high K+ excretion conditions (such as a high K+ diet)
where are ENaC channels located?
- epithelial Na+ channels are located in the DCT on principal cells
what drugs block ENaCs?
- amiloride
- triamterene
which drugs block aldo-Rs?
- spiro
- eplerenone
aldo-R blockers & ENaC blockers are considered what type of diuretics?
K+ sparing diuretics
osmotic diuretics work here:
PCT
loop diuretics work here:
LOH
thiazide diuretics work here:
DCT
anything that reduces Na+ reabsorption will also indirectly:
reduces the amount of water reabsorbed
an increase in K+ secretion
(i.e. loop diuretics or basically anything that decreases Na+ reabsorption upstream)
recall the 4 layers of the adrenal gland
- zona glomerulosa (outermost)
- zona fasciculata
- zona reticularis
- medulla (deepest)
which layer of the adrenal gland is aldosterone produced in?
zona glomerulosa
cortisol and androgens are found in this/these layers of the adrenal gland
zona fasiculata
zona reticuluaris
a small amount of estrogens are produced in this layer of the adrenal gland
zona fasciculata
the medulla of the adrenal glands produces these:
catecholamines (norepi/epi)
betwen norepi and epi, the adrenal gland medulla releases more:
epi than norepi
(4:1, epi:norepi ratio)
the higher [K+] levels, the (more/less) aldo gets secreted?
more
the lower the [K+], less aldo gets released
how does cortisol increase blood pressure?
- it is a choelsterol derivative and has cross reactivity with aldo-R’s
in principal cells, how does the cell prevent cross reactivity of cortisol and aldo-R’s?
- 11 beta-HSD type II (hydroxysteroid dehydrogenase) is an enzyme that decreases the likelihood of cortisol interacting with aldosterone-R’s
what inhibits 11-B-HSD Type II?
chinese licorice
* this compound is typically used as a licorice flavoring in tobacco
what are some systemic effects that chinese licorice has on the body?
- increases BP
- increases [K+] levels
ECF [K+] and aldosterone have a(n) indirect/direct relationship?
direct: as ECF [K+] levels increase, aldosterone increases
* the more K+ there is, the more K+ will be secreted > excreted (also the more aldosterone levels increase to help with K+ secretion)
what are the intercalated cell’s role in the DCT?
- pH regulation
what are type A intercalated cells?
- type A intercalated cells secrete protons (H+)
what are type B intercalated cells?
- these cells secrete HCO3- (via a HCO3- pump)
- they also reabsorb H+
what is the secretory process for type A intercalated cells?
- H+/ATPase pump (a strong pump capable of secreting a lot of acid)
- H+/K+/ATPase pump
contrast principal & intercalated cells in terms of location and ion movemement:
prinipal cells:
* DCT
* CD
* sensitive to ADH
* K+ management*
* water balance
intercalated cells:
* DCT
* CD
* sensitive to ADH
* pH regulation*
* water balance*
* two types: A & B
Principal: Potassium
what are V2 receptors and where are they found?
- V2 receptors bind to vasopressin
- V2 receptors are found in late distal tubule and CD
what are the effects of V2-R agonism?
- when vasopressin binds to V2-R’s, cAMP increases
- PKA becomes active
- PKA phosphorylates AQP-2 channels
- AQP-2 channels get moved to luminal membrane/apical membrane to allow more water to diffuse into the cell
ADH/vasopressin dependent type aquaporin channels:
AQP-2
found on the tubular/apical/luminal membrane
non-ADH/vaso-dependent aquaporin channels:
AQP-3 and AQP-4
found on the basolateral/interstitial membrane of cell
TAL/thin ascending limb are AKA as the _____ segment
- diluting segment
- AKA diluting segment because the TAL reabsorbs a lot of electrolytes, but not water
- this means the** tubular fluid is more dilute**
nephrogenic DI:
- problem with vaso/ADH binding/response in the kidneys
central DI:
- problem with release of ADH in the CNS
can be caused by head trauma/injury
what condition can induce nephrogenic DI?
- high serum lithium levels
- causes a loss of about 20L of urine daily
- excessive water intake to compensate for fluid loss
- can cause urine osmolarity to drop to 50 mOsm/L at the LOWEST
explain how the nephrogenic DI excessively dilutes urine:
- thin and thick ascending LOH already dilute urine (only reabsorb electrolytes)
- since tubular fluid is already dilute upstream, DCT & CD will also have trouble reabsorbing water, further diluting tubular fluid
- drops urine osmolarity to 50 mOsm/L at the absolute lowest
what are the effects of ETOH on the brain and kidney?
- decreases ADH release from brain
- impairs ability of ADH to respond to kidneys
relate vasopressin levels to water concentrations in the body:
- increased water concentrations > decrease vasopressin levels
- decreased water concentratinos > increase vasopressin levels
in terms of blood volume, contrast the role of baroreceptors vs large veins/atria of heart
- large veins/atria: concerned with low pressure/blood volume changes
- baroreceptors: concerned with high pressure/blood volume changes
the primary control system of blood osmolarity in the brain:
- osmoreceptors
where are the osmoreceptors located in the brain?
- hypothalamus
where are the two main nuclei responsible for ADH production in the hypothalamus?
- supraoptic neuron
- paraventricular neuron
5/6 of ADH production occurs here:
- supraoptic nueron
1/6 of ADH production occurs at paraventricular neuron
which part of the pituitary gland receives the ADH from the osmoreceptors?
the posterior lobe of the pituitary gland
what is the alias for the posterior lobe of the pituitary gland?
neurohypophysis
what is the alias for the anterior lobe of the pituitary gland?
adenohypophysis
adeno = anterior
a cell placed into a dilute solution would cause the cell to:
swell
ex) sol’n = 200 mOsm/L
dilute solution? cell SWELLS
a cell placed into a hypertonic solution would cause the cell to:
shrink
ex) sol’n = 360 mOsm/L
a cell placed into an isotonic solution would cause the cell to:
not change
ex) sol’n = 280 mOsm/L
cellular swelling would cause ADH levels to:
decrease its release from osmoreceptors
cellular shrinking would cause ADH levels to:
increase its release from osmoreceptors to dilute cellular osmolarity
how do the osmoreceptors interpret osmolarity changes and how do they respond to those changes?
- cells in a hypotonic solution would sense water coming into the cell to cause swelling - this would slow the rate of AP that are being sent to the osmoreceptors, causing decreased levels of ADH to be released
- cells in a hypertonic solution would sense water leaving the cell to cause shrinking - this would increase the rate of AP that are being sent to the osmoreceptors, causing increased levels of ADH to be released
if there is more ADH present, the [urine] will be:
high
(max 1200 mOsm/L)
if there is less ADH present, [urine] will be more:
dilute
(50 mOsm/L at the MINIMUM)
[urine] would be highest at what parts of the nephron?
- the deepest level of the LOH
- medullary nephron with high levels of ADH
define the role of urea in the CD:
- UT-A1 and UT-A3 transporters are located here to help conserve urea by reabsorbing it
- by reabsorbing urea, the renal interstitium can become more concentrated, which allows more fluid to be reabsorbed, thereby increasing blood volume
in a state of high ADH levels, urea transporters and AQP-2 channels would (increase/decrease)?
- UTA1 and UTA3 transporters would increase
- AQP-2 channels would also increase
- the increase in both transporters and aquaporin channels in the CD would increase the anti-diuresis effect
in terms of plasma osolarity regulation, what is the sole regulator that can selectively reabsorb water from electrolytes?
ADH
if Na+ intake goes from 30 mEq/day to 180 mEq/day with intact ADH regulation, you would expect plasma [Na+] osmolarity to be:
fairly consistent (maintaining an osmolarity of about 141-143 mEq/L)
this works in the same way with K+
if Na+ intake goes from 30 mEq/day to 180 mEq/day withOUT intact ADH regulation, you would expect plasma [Na+] osmolarity to be:
uncontrolled, with plasma Na+ concentration to range from 137 - 152 mEq/L
this works in the same way with K+
what is caffeine’s effect on ADH?
caffeine reduces ADH release from the pituitary gland
what decreases thirst?
- decreased plasma osmolarity
- increased blood volume
- increased BP
- decreased AT II
- gastric distention
what increases thirst?
- increased plasma osmolairty
- decreased blood volume
- decreased BP
- increased AT II
- mouth dryness
what decreases ADH levels?
- decreased plasma osmolarity
- increased blood volume
- increased BP
- ETOH
- clonidine (decreases BP)
- haldol (dopa blocker)
what increases ADH levels?
- increased plasma osmolarity
- decreased blood volume
- decreased BP
- nausea
- hypoxia
- morphine
- nicotine
- cyclophosphamide
what is ideal urine osmolarity in a healthy person?
600 mOsm/L
if somebody drinks 1L of distilled water, what would increase and what would decrease in terms of urine osmolarity, plasma osmolarity, urinary flow rate, and ADH levels?
- decreases:
+ADH levels d/t slight decrease in plasma osmolarity
+urine osmolarity drops as ADH drops - increases:
+urinary flow rate (to get rid of excess water ingested) - constant:
+plasma osmolarity (initially dips with water intake, but remains well regulated with ADH)
+urinary solute excretion (if no electrolytes were ingested, there is no need to get rid of extra electrolytes)
