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RENAL > A. CONCENTRATION OF URINE > Flashcards

A. CONCENTRATION OF URINE Flashcards

1
Q

how does the kidney conserve water by excreting a concentrated urine (2 ways)

A
  1. high osmolality in medullary interstitium created/maintained by LoH provides osmotic gradient for water reabsorption into peritubular capillaries
  2. action of ADH (aka vasopressin) which increases water (and urea) permeability of collecting duct

*increased water reabsorption means less urine formation (lower volume and more concentrated)

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2
Q

how does osmolality differ as you move from outer medulla to inner medulla towards pelvis of kidney

A

increases (becomes more hyper-osmotic)

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3
Q

thin descending limb

A
  • permeable to water
  • impermeable to Na+ and Cl-
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4
Q

thick ascending limb

A
  • permeable to water
  • impermeable to Na+, Cl-, HCO3-, Ca2+, K+
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5
Q

thin ascending limb (only in long LoH)

A
  • impermeable to water
  • permeable top Na+, Cl-
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6
Q

thick ascending limb reabsorption/secretion

A
  • Na+/K+ ATPase maintains low Na+ in tubular cell
  • Na+/K+/2Cl- symporter moves Na+, K+, 2Cl- across apical membrane into cell as a result of Na+ gradient
  • K+ channel in apical membrane enables K+ transported via Na+/K+/2Cl- to be recycled back
  • Na+/H+ antiporter in apical membrane enables Na+ reabsorption and H+ secretion, with HCO3- reabsorbed

*the lumen is slightly +ve, +10mV relative to interstitial fluid, creating an EC gradient for paracellular diffusion of cations between tight junctions

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7
Q

what is the osmolality of the PCT

A

isotonic (same osmolality of plasma)

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8
Q

what is the osmolality of the DCT

A

hypo-osmotic

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9
Q

what process creates the hyperosmotic medullary interstitium

A

countercurrent multiplication
- active movement of NaCl via Na+-K+ ATPase and Na+/K+/ 2Cl- symporter
- creates gradient for water reabsorption from descending limb by osmosis
- urea recycling

*Countercurrent exchange, in the long peritubular capillaries (vasa recta), preserves hyperosmolality of the renal medulla

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10
Q

countercurrent multiplication

A
  • LoH has 2 parallel limbs with tubular fluid moving in opposite directions
  • countercurrent flow “multiplies” the osmotic gradient between the tubular fluid in descending and ascending limbs, increasing osmotic gradient throughout the medulla
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11
Q

role of ADH on kidneys (vasopressin)

A
  • regulates volume and osmolality of urine
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12
Q

low ADH levels in blood

A
  • large volume of dilute urine excreted
  • diuresis
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13
Q

high ADH levels in blood

A
  • small volume of concentrated urine excreted
  • anti-diuresis
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14
Q

where is ADH synthesised

A

in neuroendocrine cells with cell bodies located in hypothalamus

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15
Q

where is ADH transported and stored

A

in nerve terminals in posterior pituitary

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16
Q

what stimulates ADH release

A
  • osmotic control: increase in body fluid osmolality
  • haemodynamic control: fall in blood volume/pressure (angiotensin II, nausea, acute stress)
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17
Q

what inhibits ADH release

A
  • atrial natriuretic peptide released from atria
  • alcohol
18
Q

ADH feedback system - osmotic control

A
  1. water deficit (dehydrated) = hyperosmotic fluid
  2. causes osmoreceptor cells in hypothalamus to shrink and get thirsty
  3. relay signal for ADH secretion from posterior pituitary
  4. ADH is transported to the kidneys and increases water permeability in late DCT & collecting duct, increasing water reabsorption
  5. correction of hyperosmotic fluid

*very sensitive mechanism = a 1% change in osmolality significantly alters ADH secretion

19
Q

ADH feedback system - haemodynamic control

A
  • decrease blood volume or blood pressure
  • activates receptors in left atrium and large pulmonary vessels
  • activates receptors in aortic arch and carotid sinus
  • (baroreceptors)
  • relay signal for ADH secretion from posterior pituitary
  • ADH is transported to the kidneys and increases water permeability in late DCT & collecting duct
  • increases blood volume and blood pressure

*less sensitive mechanism - 5-10% change in blood volume/pressure stimulates ADH secretion

20
Q

how does ADH increase water permeability

A
  • ADH binds to V2 receptor (GPCR - Gs receptor)
  • AC hydrolyses ATP to cAMP
  • inactive PKA converted to active PKA
  • protein phosphorylation of vesicles with inactive water channels (internalised AQP2) fuse with cell membrane and are now functional
  • now an increase in water permeability and increased water reabsorption
  • promotes insertion of aquaporin 2 water channels in apical membrane in P cells of late DCT and collecting duct
21
Q

what channels are on the basolateral membrane of P cells

A
  • AQP3 and AQP4 water channels
  • can’t be regulated by ADH
22
Q

what channels are on the apical membrane of P cells

A
  • AQP2 water channels
  • regulated by ADH
  • secreted by posterior pituitary
23
Q

how much NaCl and urea in outer medulla

A
  • 100% NaCl
  • 0% urea
24
Q

how much NaCl and urea in inner medulla

A
  • 50% NaCl
  • 50% urea
25
Q

how much urea is reabsorbed in PCT

A

50%

26
Q

what part of the nephron is impermeable to urea

A
  • LoH (thick ascending) and DCT so urea is carried along filtrate
  • urea conc increases along nephron and and other solutes reabsorbed
27
Q

what part of the nephron is permeable to urea

A
  • CD
  • urea diffuses down conc grad and moves into interstitial fluid, increasing its hyperosmolality
  • some urea passes from IF into thin LoH = recycling
28
Q

how does ADH affect permeability of CD to urea

A
  • increases permeability
  • increases activity & expression of urea UT-A transporters
  • more urea contributing to hyperosmolality of renal medulla
29
Q

what effect does aldosterone have on kidney

A
  • reabsorption of Na+ and water
  • secretion of K+
  • secretion of H+
30
Q

what is aldosterone secretion stimulated by

A
  • angiotensin II (RAAs)
  • increased plasma K+ conc
31
Q

what receptors does aldosterone primarily bind to

A

nuclear receptors (intracellular) - genomic effects due to affecting gene expression

32
Q

how does aldosterone cause genomic effects

A
  • diffuses across membrane as is lipophilic
  • binds to mineralocorticoid receptor (in cytosol or nucleus) which affects gene expression
  • aldosterone-included proteins like ENaC and Na+/K+ ATPase produced
33
Q

what happens when aldosterone binds to plasma membrane receptors

A
  • rapid response
  • non-genomic effects
34
Q

how does aldosterone affect P-cells of late DCT and CD

A
  • unregulated expression of Na+/K+ ATPase and ENaC
  • increased mRNA, increased translation, increased transporter pumps produced
  • increased Na+ reabsorption
  • increased water reabsorption
    (following passively)
  • increased K+ secretion (elimination) as more K+ moved into tubular cell
35
Q

how does aldosterone affect I-cells of late DCT and CD

A
  • stimulates reabsorption of bicarbonate and K+
  • secretion of H+ (through plasma membrane receptors as quick?)
36
Q

what is renin release stimulated by

A
  • decreased NaCl conc in filtrate sensed by macula densa cells (low body fluid molality)
  • decreased BP sensed by baroreceptors (pressure sensors) in afferent arterioles (low BV and hence BP)
  • Beta-ARs on granular cells through SNS
37
Q

what does increased renin release cause

A
  • increased angiotensin II production and aldosterone release
  • causes increased Na+ reabsorption and hence water retention
  • homeostasis!
38
Q

what is the RAAs a critical regulator of

A
  • blood volume
  • blood pressure
  • fluid and electrolyte balance
  • systemic vascular resistance
39
Q

what patients benefit with blockade of RAAs

A
  • hypertension
  • acute myocardial infarction
  • chronic heart failure
  • stroke
  • diabetic nephropathy
40
Q

what is the consequence of increased activation of RAAs

A
  1. increased angiotensin II
    - vasoconstriction so increased BP, increased GFR (via VC of efferent arteriole)
  2. increased aldosterone
    - increased Na+ and water reabsorption
    - increased BV and BP (increased GFR also)
    - increased K+ secretion so loss of K+ in urine = hypokalaemia
    - increased H+ secretion so loss of H+ in urine = metabolic alkalosis

RENAL (13 decks)

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