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NPB 113 > renal system > Flashcards

renal system Flashcards

1
Q

m

actions of renal system

A
  1. reconditioning of blood
    • pH, H2O content/solute [x], [Na], [K] balance
    • regulate MAP
    • limit water excretion when dehydrated
  2. get rid of waste
    • nitrogenous waste from protein breakdown
    • breakdown of products from drug or toxin
  3. important for RBC synthesis: renal system receives a lot of bf → monitors PO2 in blood & secretes erythropoietin when arterial PO2
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2
Q

bowman’s capsule

A

location of filtrate formation: liquid w/ same solute/ion composition as blood plasma except proteins

  • filtration (not exchange)
  • visceral layer = right up against bv (epithelial cells)
  • parietal layer = not against bv
  • bowman’s space in between visceral & parietal layers
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3
Q

proximal convoluted tubule (PCT)

A
  • in cortex only
  • receives filtrate from renal corpuscle
  • unregulated reabsorption (majority of reabsorption (2/3))
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4
Q

loop of henle

A

establishes standing osmotic gradient → allows us to reabsorb water

  • dissolved [solute] varies w/ depth in medulla
  • osmolarity increases towards papilla (300 → 1200 mOsm)
  • allows us to use osmosis to pull water out in DCT & CD
  • allows us to concentrate urine
  1. descending limb: unregulated reabsorption of water (towards medulla)
  2. thin ascending limb: passive reabsorption of NaCl
  3. thick ascending limb: active reabsorption of NaCl
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5
Q

distal convoluted tubule (DCT)

A
  • regulated reabsorption (also in collecting duct)
  • Na, H2O (follows solutes), Cl (follows Na)
  • regulated secretion of K
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6
Q

bowman’s capsule epithelium

A

filtration barriers prevent proteins from crossing

  • flat epithelium, normal apical membrane, squamous
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7
Q

PCT epithelium

A

FX: reabsorption ∴ need lots of SA @ apical membrane
- lots of microvilli

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8
Q

loop of henle epithelium

A
  • shows lots of heterogeneity
  • flat in descending portion
  • cuboidal in thick ascending limb
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9
Q

DCT epithelium

A

fx: reabsorption &/or secretion

  • not as much microvilli
  • less filtrate volume than PCT
  • principal cells
    • mediate Na reabsorption in response to aldosterone
    • mediate K secretion stimulated by aldosterone
    • ADH mediates H2O reabsorption (ADH = vasopressin)
    • also the cells of the collecting duct
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10
Q

renal fxs

A
  1. filtration: produces filtrate → moves solutes from blood to lumen of nephron (renal corpuscle)
  2. reabsorption: moves H2O/solutes from filtrate back into blood (PCT, descending limb of loop of henle, DCT, CD)
  3. secretion: moves stuff from blood to lumen of nephron (DCT & CD)
  4. excretion: remove urine from body
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11
Q

filtration barriers

A
  1. wall of capillaries ➞ fenestra are small enough to exclude cells (RBC, WBC, plasma proteins)
  2. basal lamina surrounding capillaries = ⊖ charged layers of proteins repels majority of plasma proteins
  3. podocytes in visceral layer of bowman’s capsule have foot processes that interdigitate & join via proteins in filtration slits that act as barrier for tiny ⊖ charged proteins
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12
Q

mesangial cells

A

cells that lie w/in glomerulus

  1. secrete extracellular matrix proteins that go into basal lamina
  2. can also contract → change shape of glomerulus & alter overall SA
    • ↑ SA → ↑ filtration rate
    • ↓ SA → ↓ filtration rate
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13
Q

primary pressure driving filtration across kidney

A

glomerular capillary hydrostatic pressure

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14
Q

ultrafiltration pressure

A

force driving fluid out of glomerulus

  • ~ 10-15 mmHg
  • never ⊖
  • PUF = Kf x [(PGC — PBS) — σ(πGC — πBS)
    • Kf = SA x Lp
      • Lp = hydraulic conductivity = how easy fluid flows through the membrane in response to pressure → influenced by size of pores/fenestra
    • σ = reflection coefficient: how easily proteins cross over the bv
      • 1 = nothing crosses over
      • 0 = crosses easily
  • depends on hydrostatic pressures (PGC — PBS)
    • PGC = stronger
      • favors filtration: pulls water across from blood to bowman’s space
      • on avg ≈ 50-55 mmHg (higher than systemic circulation)
      • influenced mainly by afferent arteriole
    • PBS = pressure due to fluids (filtrate) inside of bowman’s space
      • opposes filtration
      • filtrate constantly made but immediately drains into PCT
      • ~ 15 mmHg
  • depends on oncotic/osmotic pressures (𝛑GC — 𝛑BS)
    • 𝜋BS ≈ 0 → no proteins in normal filtrate
      • favors filtration: pulls water across from blood to bowman’s space
    • 𝜋GC due to blood proteins: albumin, fibrinogen, globulins
      • opposes filtration
      • ~ 25 mmHg (same as systemic circulation)
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15
Q

filtration through the glomerulus

A

glomerulus filters across first 1/3-1/2 of the way through, then balance between forces s.t. there is no net filtration

  • as we filter across glomerulus: PGC ↓ & 𝜋GC ↑ so balance out so no additional exchange
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16
Q

what is a normal GFR?

A

125 mL of filtrate/min

  • ≈ 20% of renal bf is converted into filtrate
17
Q

altering glomerular BP

A

afferent & efferent arterioles vasoconstrict/vasodilate (main controller = SNS)

  1. vasoconstricting afferent arteriole ➞ ↓ bf into glomerulus ➞ ↓ RBF & ↓ GFR (stronger effects)
  2. vasoconstricting efferent arteriole ➞ ↓ bf from leaving glomerulus ➞ ↑ GFR initially but ↓ GFR ultimately due to ↓ RBF
18
Q

factors influencing GFR

A
  1. hydrostatic pressures of glomerulus & bowman’s space
  2. oncotic/osmotic pressures of glomerulus & bowman’s space
  3. reflection coefficient: how easily proteins cross bv
  4. total SA → influenced by mesangial cells
    • contract → ↓ SA
    • relax → ↑ SA
  5. hydraulic conductivity (Lp) (not significantly affected by mesangial cell contractions)
19
Q

glomerular autoregulation mechanisms

A
  1. myogenic mechanism: VSM automatically contracts or relaxes as afferent arteriolar BP changes
    • ↑ afferent arteriole BP → SMC contract
    • ↓ afferent arteriole BP → SMC relax
    • not mediated by SNS
    • local response
  2. tubuloglomerular feedback
    • signal factor comes from juxtaglomerular apparatus (JGA)
      • adenosine, ATP, or thromboxane released by JGA in response to ↑ PGC & ↑ GFR (↑ in filtrate flow in DCT)
    • signal factor binds to SMC on afferent arteriole → vasoconstriction → ↓ GFR
20
Q

where does renal autoregulation occur?

A

at afferent arterioles

21
Q

goal of renal autoregulation

A
  • keeps PGC constant → keeps GFR constant
  • body sees small changes in MAP → autoregulation ensures bf into glomerulus is constant
  • ↑ MAP → vasoconstrict afferent arteriole
  • not to regulate MAP/BP
22
Q

sympathetic stimulation of renal bf

A
  • sympathetic activity overrides autoregulatory response
  • ↓ MAP detected by high-pressure baroreceptors → ↓ PSNS & ↑ SNS
  • ↑ SNS causes afferent arteriole to vasoconstrict → ↓ GFR
  • ↑ SNS activity to kidney causes ↓ renal bf (RBF)
  • ↑ SNS to efferent arteriole ↑ PGC, ↓ RBF, initial rise in GFR then ↓
    • SNS input ↓ bf in but vasoconstricting efferent arteriole keeps P in glomerulus high enough to maintain filtration for a little
23
Q

renal transport processes for H2O-soluble reabsorption

A
  1. facilitated diffusion/membrane transporter-mediated diffusion
    • uses transporter in PM
    • changes conformation
    • can be at either apical or basolateral membrane
    • requires [gradient]
    • no ATP used
  2. channels
    • only for ions
    • ions interact w/ sides/wall of channels
    • tiny → only ions can manage to get through
    • requires [gradient]
    • no ATP
  3. active mechanisms
    • ATP is used directly or indirectly
    • Na/K ATPase helps establish Na [gradients] → keeps Na inside cell very low
    • secondary active transport: allows us to move items using Na gradient
      • indirectly uses ATP
      • other items co-transport
    • primary active transport directly uses ATP
      • ex: Na/K ATPase
    • gradient does not matter
  4. endocytosis
    • ATP dependent
    • moves very big items
    • wrapped by membrane & enveloped
  • if it involves a transport protein, we only have a set # of transporters → if overwhelmed w/ substrate transporters are overwhelmed ∴ cannot be reabsorbed → excreted in urine = exceeded transport maximum
24
Q

Na reabsorption in PCT

A
  • 66-67% of filtered Na is reabsorbed
  • unregulated
  • Na/K ATPase in basolateral membrane establishes low intracellular [gradient]
  • energy of Na flowing into cell down [gradient] used to drive secondary active transport of other solutes
25
Q

K reabsorption mechanisms in PCT

A
  • majority of K
  • cannot put K channel in apical membrane → would diffuse into lumen down [K]
  1. paracellular via solvent drag: water moves via osmosis
  2. paracellular via charge gradient: ⊖ electrical charge in interstitium attracts K
26
Q

Cl reabsorption mechanisms in PCT

A
  • 66-67% of filtered Cl
  1. paracellular via attraction to Na (in early PCT)
  2. transcellular via
    1. HCO3-/Cl anion cotransporter in apical membrane in late PCT
    2. Cl channel in basolateral membrane
27
Q

glucose reabsorption mechanisms in PCT

A
  • 100% of filtered glucose
  1. requires 2º active transport using sodium-dependent glucose transporters
    1. SGLT-2: 1:1 Na:glucose → early in PCT
    2. SGLT-1: 2 Na:1 glucose → late in PCT (lower concentration of glucose later on in PCT = harder to get across)
  2. using facilitated diffusion: GLUT transporters
    • blood removes glucose from ECF which maintains [gradient]
    • no energy required
    • inslulin-independent
    • GLUT-2 → early in PCT
    • GLUT-1 → late in PCT
28
Q

hyperglycemia:

A
  • resting glucose >200 mg/dL (type I DM)
  • reabsorption of glucose is not complete (cannot remove all glucose from filtrate) transporters have hit transport maximum
  • glucose stays in filtrate ∴ water is retained in filtrate → PU/PD
29
Q

AA reabsorption mechanisms in PCT

A
  • 100% of filtered AA
  • at both apical & basolateral membrane, uses:
    1. 2º active transport
    2. facilitated diffusion transporter that changes conformation
30
Q

small peptide reabsorption mechanisms in PCT

A
  • get digested into single AA at apical membrane
  • then transported via AA mechanisms
  • albumin = exception → reabsorbed whole via pinocytosis
31
Q

function of the standing osmotic gradient

A

facilitates H2O reabsorption at:

  1. descending limb of loop of henle
    • water permeable (impermeable to solutes)
    • aquaporins
    • not hormonally regulated
  2. collecting duct
    • hormonally regulated
32
Q

Na reabsorption mechanisms in PCT

A
  1. transcellular 2º active transport occurs in early PCT
  2. paracellular via charge gradient towards end of PCT
33
Q

ascending limb of the loop of henle

A
  1. creates standing osmotic gradient
  2. filtrate becomes more hypotonic (watery)
  • osmolarity in the interstitium of the inner medulla:
    • 600 out of 1200 mOsm due to urea
    • 300 due to NaCl (300 mOsm Na+ + 300 mOsm Cl- = 600 mOsm)
  • osmolarity in the thin ascending limb:
    • 600 mOsm NaCl (600 Na + 600 Cl)
    • creates a NaCl [gradient]
  • in thin ascending limb: Na & Cl flow out passively from loop to interstitium
  • in thick ascending limb: Na (+Cl) are actively transported using Na/K ATPase at basolateral membrane
34
Q

reabsorption in the distal convoluted tubule

A

hormonally regulated reabsorption of

  1. water
  2. Na (+ Cl + water)
  • sweat → dehydration → ↑ osmolarity → reabsorb water only (need to correct osmolarity)
  • hemorrhage → blood volume loss → reabsorb water + NaCl (no change in osmolarity so no need to correct it)
35
Q

osmolarity in DCT

A

H2O reabsorption causes filtrate to rise to 300 mOsm
- filtrate at beginning of DCT (coming out of loop of henle) = 100-180 mOsm (majority = Na, some Cl, K)
- in cortex = 300 mOsm
- ∴ pulling water across from filtrate to cortex
- filtrate osmolarity increases as it flows through DCT & CD → allows us to concentrate urine & prevent water loss/dehydration

36
Q

kidney response to dehydration

A

blood plasma osmolarity ↑ due to water loss

  • detected by osmoreceptors in hypothalamus
  • releases ADH (vasopressin) from posterior pituitary
    • also associated w/ thirst drive
    • acts on principal cells in DCT & CD
    • inserts AQP-2 in apical membrane of principal cells → recruits vesicles holding AQP-2 in membrane fuse w/ apical membrane
    • AQP-1 & AQP-3 always present & open in basolateral membrane → not under hormonal regulation
    • P w/ hypertension tx w/ diuretics → prevents additional insertion of AQP-2 channels → excrete more water

NPB 113 (5 decks)

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