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60 Cards in this Set

  • Front
  • Back
range of osmolarity of urine that can be excreted by kidney
50 mOsm/L to 1200-1400 mOsm/L
action of ADH
increase permeability of distal tubules and collecting ducts to water
net consequence of ADH
large amount of water reabsorbed, decreased urine V, but doesn't markedly change the rate of renal excretion of the solutes
what is the osmolarity of fluid leaving the early distal tubule
~100 mOsm/L regardless of ADH concentration (hypo-osmotic, plasma is 3 times more)
why does severe dehydration occur by drinking seawater
seawater has osmolarity around 1000-1200 mOsm/L, max kidney urine concentration ability is 1200 and the kidney has to get rid of more solutes than just the components of the seawater (at least 600 mOsm/day)
components required for concentrated urine
1)ADH 2) high osmolarity of renal medullary interstitial fluid
vasa recta
specialized peritubular capillaries of the renal medulla
Major factors that contribute to the build-up of solute concentration in the renal medulla
1) active Na+ transport and co-transport of other electrolytes out of thick ascending and loop of Henle 2) active transport of ions from collecting ducts 3) facilitated diffusion of urea into interstitium 4) diffusion of only small amount of water from medullary tubules into interstitium
why is the osmolarity difference of the thick ascending loop max out around 200 mOsm/L
paracellular diffusion of ions back into the tubule eventually counterbalances transport of ions out
countercurrent multiplier
repetative reabsorption of NaCl by the thick ascending loop of Henle and contiued inflow of new NaCl from the proximal tubule into the loop of Henle
what preserves high medullary interstitial fluid osmolarity when water is reabsorbed (especially in presence of ADH)
reabsorbed into the cortex where it is swept away by rapidly flowing peritubular capillaries
what percent of renal medullary interstitium osmalarity is urea responsible for
~40-50%
how is urea reabsorbed
passively in inner medullary collecting ducts
what is the urea transporter UT-AI activated by
ADH
malnutrition and urea concentration ability
low in medullary interstitium and considerable impairment of urine concentration ability
how much of the filtered load of urea is usually excreted
20-50%
what determines rate of urea excretion
1) concentration of urea in plasma 2) glomerular filtration rate (GFR)
where is 40-50% of filtered urea reabsorbed
proximal tubule
what areas are fairly urea impermeable
thick limb, distal tubule, and cortical collecting tubule
how can urea circulate through the terminal parts of the tubular system
secreted into thin loop of henle and is reabsorbed in collecting duct
Two special features of vasa recta that preserves high solute concentrations
1)medullary blood flow is low 2) serve as a countercurrent exchange minimizing washout
what can increase blood flow in renal medulla and 'wash-out' solutes
vasodilators, high arterial P
reabsorption in porximal tubule
~65% filtered electrolytes reabsored here, but water follows
descending loop permeabilities
water, less to NaCl and urea
thin ascending limb permeabilities
not to water; reabsorbs some NaCl and urea
thick ascending limb permeabilities
not to water; large amounts of NaCl, K+ actively transported into interstitium; 100 mOsm/L filtrate
what does low Na+ concentration in body stimulate
angiotensin II and aldosterone
osmolar clearance
volume of plasma cleared of solutes per minute
osmolar clearance formula
Cosm = Uosm x V / (Posm); Uosm is urine osmolarity, V is urine flow rate, and Posm is plasma osmolarity
Free water clearance
represents rate at which solute-free water is excreted by the kidneys; difference btwn water excretion (urine flow rate) and osmolar clearance
what does a pos/neg free water clearance mean
pos = excess water being excreted; neg = excess solutes being removed
what can impair ability to concentrate urine
1) inappropriate ADH secretion 2)impairment of countercurrent mechanism 3) inability of distal tubule, collecting tubule, and collecting ducts to respond to ADH
another name for failure to produce ADH
central' diabetes insipidus
what can cause central diabetes insipidus
head injuries, infections, congenital
central diabetes insipidus treatment
synthetic ADH called desmopressin
what does desmopressin act on
selectively on V2 receptors to increase water permeability in late distal and collecting tubules
another name for inability of kidneys to respond to ADH
nephrogenic' diabetes insipidus
what can cause nephrogenic diabetes insipidus
failure of countercurrent mechanism; failure of distal and collecting tubules to respond to ADH
how do diuretics impair concentrating ability
inhibit electrolyte reabsorption
what drugs can impair kidney response to ADH
lithium and tetracyclines
plasma Na+ concentration
140-145 mEq/L
Plasma osmolarity rough calculation
Posm = 2.1 x Plasma Na+ concentration
why does urea exert little effective osmotic P under steady state conditions
easily permeates most cell membranes
Two primary systems involved in regulating concentration of Na+ and osmolarity of ECF
1) osmoreceptor-ADH system 2) thirst mechanism
where are osmoreceptor cells
anterior hypothalamus near the supraoptic nuclei
what occurs when osmoreceptor cells shrink
causes them to fire relaying signals down stalk of pituitary gland to posterior pituitary
magnocellular neurons in the hypothalamus that synthesize ADH
supraoptic and paraventricular nuclei
how rapidly can ADH be secreted
rapidly; plasma ADH levels can increase several fold within minutes
anteroventral region of the third ventricle contains
subfornical organ on upper part, inferior is organum vasculosum, and in the middle s the median preoptic nucleus
connections of the median preoptic nucleus
supraoptic nucleu and BP control centers in the medulla
what cardiovascular reflexes can control ADH secretion
1)arterial baroreceptor reflexes 2) cardiopulmonary reflexes (aortic arch and carotid sinuses, cardiac atria)
what nuclei are P refexes sent to from the glossopharyngeal and vagus nerves
tractus solitaris
what drugs stimulate ADH release
nicotine, morphine; (alcohol inhibits)
thirst center
anteroventral wall of 3rd ventricle
angiotensin II and thirst
acts on organum casculosum
how long is required for water to be absorbed once ingested
30-60 minutes
angiotensin II and aldosterone effect on sodium concentration
little effect except under extreme conditions due to water reabsorption along with Na+
Addisons and sodium concentration
lack of aldosterone leads to sodium wasting, thirst mechaism compensates for volume loss, but not Na+ loss
average industrial Na+ intake vs necessary intake
100-200 mEq/day vs 10-20 mEq/day
two primary stimuli for salt appetite
1) decreased ECF Na+ concentration 2) decreased blood V or BP; similar neuronal mechanisms as thirst mechanism