7. Renal transport mechanisms Flashcards

1
Q

why filter 180L/day and reabsorb 99%?

A
  1. foreign substances are filtered into the tubule but not reabsorbed into the blood
  2. filtering ions and water into the tubule makes regulation simple
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2
Q

what plays the biggest role in the reabsorption capabilities of the proximal convoluted tubule?

A

Na/K ATPase in the basolateral membrane

all reabsorption is somehow linked to this transporter

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3
Q

how much of the filtrate is reabsorbed in the PCT

A

approx. 67%

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4
Q

where is the energy needed for antiport derived from?

A

usually Na/K ATPase

creates gradient needed for one molecule to assist in the transportation of another in the opposite direction

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5
Q

how is chloride reabsorbed

A

Passive paracellular movement

as filtrate is moving down the PCT, more water and sodium are being reabsorbed than chloride. by the later segment of the proximal tubule, concentration of chloride rises by ~20%. this creates a concentration gradient and allows for passive paracellular chloride movement

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6
Q

what determines paracellular movement of water

A

presence or the absence of tight junctions between cells

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7
Q

where are aquaporins present

A

transcellular route for water

AQP-1 (proximal tubule absorbs 65-70%)
AQP-2 (CD under the control of ADH)

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8
Q

net water permeability of the renal tubules is determined by what two factors

A

presence or absence of tight junctions (paracellular)

presence or absence of aquaporins (transcellular)

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9
Q

two types of sodium-coupled glucose transporters

A

SGLT-1 (3rd section of PCT; absorbs 10% of glucose)
SGLT-2 (1st and 2nd section of PCT; absorbs 90% of glucose)

ACTIVE transport

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10
Q

what is the transport maximum (Tm) of glucose

A

375mg/min = plasma glucose of about 200mg/dL

anything above this is not reabsorbed, but excreted in urine

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11
Q

where are the NK2Cl cotransporters located

A

thin and thick ascending loop

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12
Q

how does furosemide work

A

loop diuretic

inhibits NaK2Cl cotransporter in thick asacending loop
inhibits NaCl reabsorption by competing for the Cl- binding site on the carrier

decreased reabsorption of Na, K and Cl
diuresis

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13
Q

Distal tubule (DCT)

A

no K reabsorption
NaCl cotransport
relatively impermeable to water (early is late isn’t)

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14
Q

Thiazide diuretics

A

blocks NaCl symporter (reabsorption in cortical segment of DCT)
increases NaCl excretion
enhance Na Ca exchange (enhancing Ca reabsorption)

natriuresis and decreased BV and BP

useful in treating calcium-subtype of kidney stones and may be useful for treating osteoporosis

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15
Q

collecting ducts

A

impermeable to water without ADH

aldosterone “fine-tunes” Na reabsorption (targets principal (light) cells)

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16
Q

urea reabsorption

A

proximal and inner medullary collecting duct can reabsorb (most by inner med)

inner medullary utilizes UT-A(special urea transport protein) which is stimulated by ADH

17
Q

what is aldosterone released in response to

A

angiotensin II or increased plasma K

always promotes increased Na reabsorption and K secretion

18
Q

hormones that decrease H20 and NaCl reabsorption

A

[ANP, BNP, urodilatin] (CD), [uroguanylin, guanylin] (PT/CD), dopamine (PT)

19
Q

hormones that increase H20 and NaCl reabsorption

A

[Angiotensin II, sympathetic nerves] (PT/TAL/DT/CD), Aldosterone (TAL/DT/CD)

20
Q

hormone that increases H20 reabsorption

A

AVP (vasopressin) (DT/CD)

21
Q

K sparing Spironolactone

A

aldosterone-dependent k sparing diuretic

inhibits Na/K exchange in DT/CD promotes K retention and Na and water loss.

hypotensive