B5-041 Renal Physiology IV Flashcards
what receptor does ADH bind to to cause vasocontriction?
V1
triggers Ca2+ release –> actin-myosin coupling –> vasoconstriction
do V1 or V2 receptors have a higher affinity for ADH?
V2 has higher affinity
thats why osmolarity causes big changes in ADH and pressure only small
small cell lung carcinoma and lung infections can cause
SIADH
secretes peptides similar to ADH, too much ADH
central Diabetes insipidus causes water diuresis because
hypothalmus does not secrete ADH
decreased water absorption, urine dilution
nephrogenic diabetes insipidus causes water diuresis due to
mutation in V2 (lithium ingestion)
decreased water reabsorption, urine dilution
diabetes mellitus causes […] diuresis
solute or water
solute
how does a normal individual react to a water restriction test?
osmolarity increases, volume decreases
primary polydipsia would be similar
how does an individual with central diabetes insipidus react to a water restriction test?
- very little change in volume/osmolarity until ADH is added
- then, osmolarity will go up and volume wil go down
how does an individual with nephrogenic diabetes insipidus react to a water restriction test?
kidneys do not respond to ADH
treatment for diabetes insipidus
ADH analog
(desmopressin)
treatment of SIADH
treat underlying cause or inhibit V2 receptors
4 main effector pathways regulating salt and water excretion
- ADH
- natriuretic peptides
- RAAS
- sympathetic nervous system
stimulus for release of ANP
increased heart volume
released from atria
stiumulus for release of BNP
increased heart volume
released from ventricle
stimulus for release of CNP
increased intravascular volume
released from brain
stimulus for release of urodilatin
increased volume and Na+ load
released from kidney
describe the mechanism of action of natriuretic peptides
- bind to NPR on vascular smooth muscle cells
- diminish calcium
- cause vasodilation
inhibits ENac in the collecting duct causing less sodium reabsorption
more dilute urine
urodilatin
how does sympathetic nervous activity regulate GFR?
produces vasoconstriction
constrict vessels –> less volume in afferent arteriole –> low GFR
sensors that regulate ECF volume
2
baroreceptors
volume receptors
sensors that regulate ECF osmolarity
hypothalmic osmoreceptors
effector pathways for regulation of ECF volume
4
- ADH
- ANP
- RAAS
- SNS
effector pathways that regulate ECF osmolarity
2
- ADH
- thirst
all transport in the proximal tubules is associated with
Na+
the proximal tubule gets rid of bicarb through
bicarb-sodium transporter in basolateral membrane
what cells in the distal and collecting tubules regulate pH?
a intercalated
how do cells a intercalated cells get rid of H+?
H+ active transporters on the apical side of cells
require ATP
for every proton that comes out, one […] comes in
bicarbonate
what cells are very important for getting rid of H+ and protect from acidosis?
a intercalated cells
what cells are very important for getting rid of bicarbonate and protecting from alkalosis?
b intercalated cells
transporter on apical side of b intercalated cells
HCO3/Cl- exchanger
basolateral in a- intercalated cells
transporter on basolateral side of b-intercalated cells
active H+ transport pump
apical in a-intercalated cells
what part of the tubule reabsorbs 80% of bicarb through Na/HCO3 transporter in the basolateral membrane?
proximal tubule
how does the kidney buffer urine?
- combine H+ with HPO4 to make phosphoric acid
- combine H+ with HCO3 to make carbonic acid
urine acidification
how does the kidney produce ammonium?
- glutamine –> glutamate = a-ketoglutarate + NH3
- NH3 combines with H+ to make ammonium (NH4)
how to calculate urine anion gap
(Na + K) - Cl
should be a negative number
urine anion gap is an indicator of the ability of the kidney to
- produce ammonium
- get rid of protons
if the UAG is negative, what does this mean?
urine anion gap
normal
kidneys are producing ammonium and eliminating H+ appropriately
equation for plasma anion gap
Na - (Cl + HCO3)
normal anion gap
8-16
what does a normal anion gap indicate?
kidneys are eliminated excess fixed acids
plasma anion gap […] as pH is reduced
increases
what cells work to compensate for alkalosis?
b- intercalated cells
if PCO2 rises, proton secretion becomes dominant and the kidney excretes […]
acid
raises blood pH
if HCO3 in plasma rise, HCO3 filtration increases and the kidney excretes […]
alkali
reducing blood pH
how does the kidney respond to respiratory acidosis?
- excretes protons in the proximal and distal portions of the nephron
- reabsorbs bicarb (bicarb raised in plasma)
- pH normalizes
how will the kidneys respond to respiratory alkalosis?
excrete bicarb (through saturation and b- intercalated cells)
causes of metabolic acidosis with normal PAG
- bicarb loss (diarrhea, proximal renal tubular acidosis)
- decreased acid secretion/bicarb consumption (distal renal tubular acidosis, aldosterone deficiency)
causes of metabolic acidosis with high PAG
- high acid input (keto acidosis, lactic acidosis, salicylate, methanol, ethylene glycol)
- low acid input (renal failure)
- decreased distal acidification
- low plasma bicarb
- normal PAG
- low serum K
- urine pH > 5.5
type I
distal RTA
- decreased bicarbonate reabsorption
- very low plasma bicarb
- normal PAG
- low serum K+
- normal/low urine pH
type II
proximal RTA
- decreased aldosterone
- low plasma bicarb
- normal PAG
- high serum K+
- normal/low urine pH
type IV
distal hyperkalemic RTA
with more aldosterone, you have more […] secretion
hydrogen
if you have hyperaldosteronism, will cause
alkalosis
if you have high aldosterone, the patient will become
alkalotic
in a patient who is hypoventilating due to chronic lung disease, the kidneys will respond by
increasing net secretion of acid
H2PO4, CO3H2, NH4+
in a patient who is hypoventilating, the PCO2 will
increase
an increase in PCO2 will activate […] in the kidney
mechanism involved in acid secretion
PCO2 is an important regulator of the activity of […] in intercalated cells
H-ATPase
actively secretes protons into the tubular lumen
H-ATPase
for each proton excreted, one […] is reabsorbed
bicarbonate
when excretion of NH4+ is adequate, the UAG is
negative
patients with type I distal renal tubular acidosis have an inability to secrete
protons
reduces amount of NH4+, UAG positive
what 2 molecules are low in urine in RTA?
bicarb
ammonium
bicarb reabsorption in the proximal tubule is tightly coupled to
secretion of protons by Na-H exchanger
a positive urine anion gap indicates
inappropriate excretion of ammonium
secreted by JG cells in response to decreased renal perfusion pressure
renin
increases renal sympathetic discharge (B1 effect) and decreases NaCl delivery to macula densa cells
renin
catalyzes conversion of angiotensin I to angiotensin II
ACE
produced by vascular endothelial cells in the lung
ACE
helps maintain blood pressure and blood volume
angiotensin II
affects baroreceptor function; limits reflex bradycardia which would normally accompany its pressor effects
angiotensin II
released from atria and ventricles in response to increased volume
ANP, BNP
- inhibits RAAS system
- relaxes vascular smooth muscle via cGMP to increase GFR and decrease renin
- dilates afferent arteriole
ANP, BNP
primarily regulates serum osmolality
ADH
stimulates reabsorption of water in collecting ducts
ADH
stimulates reabsorption of urea in collecting ducts to maximize corticopapillary osmotic gradient
ADH
primarily regulates ECF volume and Na+ content
aldosterone
- release is increased in hypovolumic states
- responds to hyperkalemia by increasing K+ excretion
aldosterone
how to beta blockers inhibit renin release?
inhibit B1 receptors in JG cells causing decreased renin release
