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Renal > Osmoregulation and Vasopressin System > Flashcards

Osmoregulation and Vasopressin System Flashcards

1
Q

Osmolarity

A
  • the concentration of discrete solute particles in solution.
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2
Q

Isosmotic

A

having the same osmolarity as plasma (but can also refer to comparison with fluids other than plasma). The prefixes hypo- and hyper- refer to osmolarities below or above that of normal plasma.

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3
Q

Diuresis

A

urine flow above usual levels

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4
Q

Water Diuresis

A

increased urine flow due to decreased reabsorption of “free” water (i.e. water without solute).

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5
Q

Antidiuresis

A
  • low rate of water excretion (usually <0.5 ml/min) as hyper-osmotic urine
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6
Q

Natriuresis

A

rate of urinary Na+ excretion above usual levels

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7
Q

Antinatriuresis

A

low rate of Na+ excretion

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8
Q

Regulation of ADH/Vasopressin Release

A
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9
Q

Regulation of Plasma [ADH] by Osmotic and Volume Stimuli

A
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10
Q

Collecting Duct Water Permeability is regulated by…

A
  • ADH – Anti Diuretic Hormone also called vasopressin
  • Activates the insertion of the water channel, aquaporin-­2, into the apical membrane of the collecting duct
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11
Q

Formation of a concentrated urine: reabsorption of UREA in medulla

A
  • Urea (and chloride) are passively moved along the proximal tubule, “dragged” through the membranes as water and salt move
  • Most membranes with leaky tight junctions are permeable to urea
  • As we progress from proximal to distal nephron, leaky “tight” junctions become tighter, now urea absorption is regulated
  • Involved in concentrating mechanism, i.e. involved in the formation of a hyperosmotic urine (bright yellow!)
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12
Q

Proximal Tubule

A
  • AQP-1 in both apical and basolateral membranes → very high transcellular hydraulic conductivity → a very small osmotic gradient (6 mOsm) can drive substantial water flow across these cells. Solute reabsorption establishes the osmotic gradient.
  • Some water crosses the epithelium via the paracellular pathway (through “leaky” junctional complexes)
  • Starling forces drive water from interstitium into peritubular capillary blood.
  • Net effect: Tight coupling of solute and water transport across this highly water-permeable epithelium; 67% of filtered Na+ and water are reabsorbed in essentially isotonic proportions (iso-osmotic reabsorption)
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13
Q

Loop of Henle

A

•Descending Thin Limb – relatively high hydraulic conductivity (due to presence of AQP-1) allows water to move out of the lumen down an osmotic gradient.

-Note: There is only minimal active solute transport by these cells, so the osmotic gradient must be established by transport activity of other cells (Thick Ascending Limb)

•Thick Ascending Limb and Distal Convoluted Tubule: water-impermeable at all times (virtually no AQP present)

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14
Q
A
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15
Q

Collecting Duct

A
  • Modulation of Water Permeability by Antidiuretic Hormone (ADH)
  • Junctional complexes in the CD are “tight” –> no paracellular water reabsorption.
  • In the absence of ADH: collecting cells are impermeable to water (AQP-3 and AQP-4 are present in the basolateral membrane, but no AQP is present in the apical membrane).
  • In the presence of ADH: Clusters of AQP-2 are inserted into the apical membrane (cAMP-dependent) –> cells become water-permeable –> allows transcellular water reabsorption.
  • Net effect: ADH can regulate water reabsorption by the collecting duct, which provides the opportunity to regulate water excretion (independent of solute excretion).
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16
Q

AQP-1

A
  • Cloned from RBCs; Present in many tissues, especially the apical basolateral membranes of the proximal tubule and descending thin limb
  • AQP-1 knockout mice have low proximal tubule water permeability
17
Q

AQP - 2

A
  • Apical membrane and intracellular vesicles in principal cells of the connecting tubule and collecting duct
  • X-linked nephrogenic diabetes insipidus
18
Q

AQP-3

A
  • Basolateral membrane of principal cells in the connecting tubule and collecting duct
  • AQP-3 knockout mice have low water permeability of the collecting duct
19
Q

AQP-4

A
  • Basolateral membrane of principal cells in the inner medullary collecting duct
  • AQP-4 knockout mice have low water permeability of the collecting duct
20
Q

Poorly-Reabsorbable Solutes Impede H2O Reabsorption

A

As a result of H2O reabsorption, filtered solutes that are poorly reabsorbable (“trapped” in the tubular lumen) become increasingly concentrated as they travel along the nephron. This process results in retaining osmotically obligated H2O in the tubular lumen, producing a diuresis.

  • This type of diuresis is termed an osmotic diuresis, and is characterized by excretion of a largerthan-normal volume of urine that is rich in solutes.
  • Poorly-reabsorbable solutes that produce an osmotic diuresis are termed osmotic diuretics.
  • Examples:
    1. Glucose (when the filtered load exceeds the Tm for glucose. Glucose not reabsorbed by the end of the proximal tubule is poorly reabsorbable in the remainder of the nephron, retaining water in the tubular fluid and resulting in an osmotic diuresis. Individuals with poorly-controlled diabetes mellitus typically exhibit a glucose-dependent osmotic diuresis.
    2. Mannitol
21
Q

Response to Water Intake

A
  • The kidneys have a critical ability to vary relative proportions of solutes and water excreted in the urine, as needed to achieve solute and water balance.
  • Excess TBW –> urine osmolarity can get as low as 50 mOsm/L

*Water deficit –> urine osmolarity can increase to 1200 mOsm/L

• These changes occur rapidly, in the absence of major alterations in plasma osmolarity, and without major changes in solute excretion.

22
Q

Response to Water Intake – Formation of Hypo-osmotic (dilute) Urine

A
  • Proximal tubule – “isosmotic” reabsorption of Na+ and water; fluid entering the loop of Henle is ≈300 mOsm/L
  • Water leaves the water-permeable descending thin limb of the loop of Henle under the influence of increasing interstitial osmolarity (“medullary interstitial osmotic gradient”). Na+ is not reabsorbed here.
  • At the bend of the loop, tubular fluid is concentrated due to water reabsorption (osmolarity is the same as the medullary interstitium).
  • The entire remainder of the nephron is impermeable to water! Therefore, all water remaining in the tubule at the bend of the loop of Henle will be excreted in the final urine. However, solute reabsorption can occur.
  • Some Na+ reabsorption occurs by diffusion as tubular fluid moves through the ascending thin limb into a progressively more dilute interstitium.
  • The thick ascending limb reabsorbs Na+ (Na+-K+-2Cl– cotransporter), but no water. The tubular fluid is diluted (solute is removed, water remains) as it traverses this segment.
  • Tubular fluid entering the distal convoluted tubule is hypo-osmotic (≈100 mOsm/L). • In the distal convoluted tubule, connecting tubule and collecting duct, additional active Na+ reabsorption (without water) further dilutes tubular fluid.

Net effect: Final urine can have an osmolarity as low as 50 mOsm/L (VERY DILUTE). Water can be excreted far in excess of solute! (This means that as little as 0.6% of filtered Na+ can be excreted together with up to 15% of filtered H2O!)

23
Q

Response to Dehydration – Formation of Hyper-osmotic (Concentrated) Urine

A
  • Requires ADH to render the distal tubule and collecting duct permeable to water.
  • Processes from the glomerulus to the beginning of the distal tubule are identical to those that occur in formation of dilute urine.
  • The hypo-osmotic tubular fluid entering the water-permeable (due to ADH) cortical collecting duct comes under the influence of a 300 mOsm/L (isosmotic) cortical interstitium. Water reabsorption occurs together with Na reabsorption. An isosmotic tubular fluid enters the medullary collecting duct.
  • The medullary collecting duct is also water-permeable under these conditions (due to ADH), and it acts as an osmotic equilibrating device. Tubular fluid traveling through the medullary collecting duct comes under the influence of the medullary interstitial osmotic gradient. Water is reabsorbed down the very large osmotic gradient. Na+ (and urea) reabsorption also occur, contributing to the osmotic gradient.
  • Maximum osmolarity of the final urine = the osmolarity of the inner medullary interstitium at the end of the collecting duct (near the papilla).

Net effect: Under the influence of ADH, a small volume of concentrated urine is formed. Compared to the formation of dilute urine, there is less water excreted (due to reabsorption in the distal tubule and collecting duct) but the same amount of solute is excreted (0.6% of filtered Na+).

24
Q

Role of Urea in the Concentrating Mechanism

A
  • In the presence of ADH, the inner medullary collecting duct becomes permeable to urea, which is passively reabsorbed into the interstitium by diffusion.
  • Some of this urea diffuses into tubular fluid in the ascending thin limb, but it is effectively “recycled” as it is consequently reabsorbed again when it reaches the inner medullary collecting duct. •

Net effect: Urea recycling contributes about 40% of inner medullary solute, reinforcing the interstitial osmotic gradient under when concentrated urine must be formed (under the influence of ADH).

25
Q

The ability of the kidney to control the osmolarity of the urine (concentrated or dilute) requires three processes that function in concert:

A
  1. The function of the loops of Henle as countercurrent multipliers to establish an osmotic gradient that increases from the cortex to the tip of the papilla.
  2. The function of the vasa recta as countercurrent exchangers to help maintain this gradient.
  3. The function of antidiuretic hormone to alter the permeability of the cortical and medullary collecting ducts to water.
26
Q

Countercurrent Multiplication in Loops of Henle

A
  • Responsible for establishing the medullary interstitial osmotic gradient
  • Requirements:
  • Countercurrent flow – flow in opposite directions through adjacent structures (loops of Henle)
  • Different water permeability of the adjacent structures having countercurrent flow (descending thin limb is water permeable; ascending limb is water impermeable)
  • Source of energy – active transport (Na+-K+-2Cl– cotransport / Na+-K+-ATPase system for reabsorption of Na+ in thick ascending limb)

• Effect of “loop diuretics”

  • Inhibition of Na+-K+-2Cl– transport
  • loose the ability to dilute tubular fluid as it passes through the thick ascending limb.
  • The medullary interstitial osmotic gradient dissipates (due to removal of the energy source necessary for countercurrent multiplication).

Net effect: Cannot form a concentrated urine; limited ability to form a dilute urine.

27
Q

Countercurrent Exchange in the Vasa Recta

A
  • Countercurrent exchange requires countercurrent flow, but does not require a permeability difference between structures with countercurrent flow, nor does it require an energy source. It is a passive process involving diffusion and osmosis. • Vasa recta are permeable to both water and solute.
  • Water is “shunted” from descending vasa recta to the ascending vasa recta. This process is most evident in the outer medulla, minimizing blood flow through inner medullary vasa recta.
  • Solute diffuses from the ascending vasa recta into the descending vasa recta. This process “traps” solute in the medulla.
  • Net effect: Minimizes washout of the medullary interstitial osmotic gradient via the vascular system.
  • Any factor that increases medullary blood flow tends to wash out interstitial solute –> diminish the medullary interstitial osmotic gradient –> decrease the ability to produce an osmotically concentrated urine. Note that ADH decreases medullary blood flow, which helps to preserve (or enhance) the concentration gradient.
28
Q

Regulation of ECF Osmolarity by AVP/ADH

A

Synthesis & Release of ADH ( ≡ AVP)

  • Synthesized in supraoptic and paraventricular neurons of the hypothalamus. • Transported along axons (hypothalamic-hypophysial tract) to the posterior pituitary, where it is stored in nerve endings.
  • Activation of supraoptic and paraventricular neurons (by appropriate stimuli) –> ADH release from nerve terminals in posterior pituitary –> enters the systemic circulation –> target cells: distal tubule and collecting duct
29
Q

Regulation of ADH Release

A

• Osmoreceptors

  • Increases in plasma osmolarity (sensed by hypothalamic osmoreceptors) stimulate ADH release. Decreased plasma osmolarity inhibits ADH release.
  • Very small changes in plasma osmolarity are able to cause significant changes in ADH release.
  • Plasma ADH levels can be altered about 10-fold as a result of changes in plasma (ECF) osmolarity.
  • Thus, osmoreceptors are sensitive (precise) regulators of ADH release. • •Baroreceptors Receptors
  • A decrease in blood volume (sensed by baroreceptors in the cardiac right atrium) can increase plasma [ADH]. Increases in blood volume above normal do not reduce plasma ADH concentration.
  • A very large (>10%) decrease in blood volume is required before any change in plasma [ADH] is evident.
  • Plasma [ADH] can increase as much as 50-fold in response to blood volume depletion.
30
Q

Increase ADH Secretion

A
  • nausea
  • vomiting
  • nicotine
  • morphine
  • Cyclophosphamide (chemotherapeutic agent)
31
Q

Decrease ADH Secretion

A
  • alcohol
  • Clonidine (antihypertensive)
  • Haloperidol (dopamine blocker)
32
Q

Syndrome of Inappropriate ADH (SIADH)

A
  • Excessive ADH secretion for any given POsm
  • Patients retain water in excess of solute, resulting in decreased POsm (hyponatremia)
33
Q

Diabetes Insipidus (DI)

A
  • Patients produce a large volume of dilute urine, even during fluid deprivation, resulting in increased POsm (hypernatremia) 
  • Two Varieties  Neurogenic (or Central) DI – Failure of ADH secretion
34
Q

Important Distinctions relative to Na+ and H2O Balance:

A
  • Alterations in sodium balance are manifest as changes in ECF volume (“volume depletion” or “volume expansion”).
  • Alterations in water balance are manifest as changes in POsm and are measured as changes in PNa. Therefore, disturbances of water balance are evident as follows:
  • Hypernatremia (PNa > 145 mEq/L) – a deficit of H20 relative to salt (“dehydration”)
  • Diabetes Insipidus (Central or Nephrogenic)
  • Hyponatremia (PNa < 135 mEq/L) – an excess of H20 relative to salt
  • Syndrome of Inappropriate ADH secretion (SIADH)
  • Nephrogenic DI – Kidney is unresponsive to ADH

Renal (26 decks)

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