Loop of Henle and Collecting Duct--Muster

Question 1

Descending tubule function

Answer 1

boring

only H₂0

drawn out of tubule into intersitium

Question 2

Osmolarity of interstitium in descending limb

Answer 2

high

~1200 mOsm

Question 3

Ascending tubule function

Answer 3

NKCC₂ transporter

Question 4

Limiting molecule in NKCC₂ transporter

Answer 4

K⁺

recycled via leak channel

Question 5

Prototypical loop diuretic drug

Answer 5

furosemide

targets NKCC₂ transporter in ascending limb

Question 6

Transporter that brings Cl^- into interstitium in ascending limb

Answer 6

K⁺/Cl^- symporter

Question 7

% Na⁺ absorbed in distal tubule

Answer 7

5%

Question 8

Distal tubule main transporter

Answer 8

Na⁺/Cl^- symporter

Question 9

Transporter(s) that moves Na⁺ and Cl^- into interstitium in distal tubule

Answer 9

Na⁺ and Cl^- leak channels

Question 10

Drug targeting distal tubule

Answer 10

hydrochlorothiazide

Question 11

Section(s) of nephron with variable/controlable absorbtion

Answer 11

collecting duct

~5%

Question 12

Collecting duct cell types

Answer 12

principle cells (Na⁺, K⁺, Cl^-)

intercalated cells (H⁺, HCO₃^-)

Question 13

What controls the 0-4.9% reabsorption of Na⁺ in collecting duct?

Answer 13

RAAS system

Question 14

How does RAAS affect the collecting duct?

Answer 14

aldosterone crosses into principle cell, binds to SRE (steroid response element)

SRE activates Na⁺/K⁺ ATPase

and

increases transcription of ENaC (endothelial Na⁺ carrier) and ROMK (renal outer medullary K⁺ channels)

Question 15

Aldosterone released in what metabolic states?

Answer 15

hyponatremia

hyperkalemia

Question 16

K⁺-sparing diuretics

Answer 16

spirinolactone, eplerenone

triamterine, amiloride

Question 17

Spironolactone

Eplerenone

MOA

Answer 17

aldosterone antagonists at

SRE (steroid response element)

reduce transcription of ENaC and ROMK

Question 18

Alosterone release

situations

Answer 18

1˚: hyponatremia or hyperkalemia

2˚: RAAS system activation

Question 19

How does aldosterone activation primary (through hyponatremia or hyperkalemia) differ from RAAS system activation?

Answer 19

AT II from RAAS blocks ROMK

(prevents potassium wasting)

ENaC not blocked when aldosterone is released due to hyponatremia/hyperkalemia