Hormones Regulating Water and Electrolytes

How is water reabsorbed in PCT

Na/K ATPase pumps Na out → creates a gradient → Na comes back in with glucose, water etc

How is water reabsorbed in thin descending limb

Permeable to water, solute impermeable

How is water reabsorbed in distal tubule

NOT water permeable unless ADH present; ADH increase water reabsorption

How is water reabsorbed in collecting duct

ADH stimulate AQP2; aldosterone stimulate Na reabsorption → Water reabsorbs too; ANP decreases Na reabsorption → water excretion

What is the effect of ADH

ADH → Bind to V2 on principal cell of DT and CD → Create AQP2 → Water reabsorption

What controls ADH release

TRPV receptors; increase vasopressin and thirst in hyperosmolar conditions

How does urine, plasma Osm, urine flow rate and urine solute excretion change in water loading

Urine Osm increase, plasma Osm constant; urine flow rate increase, urine solute constant

What happens during water deprivation

ADH level increase, renal medulla has high osmolarity → Increased water reabsorption

What is central diabetes insipidus

Inability for the hypothalamus to produce ADH

What is peripheral/nephrogenic diabetes insipidus

Kidney does not respond to ADH ; ADH production normal

What is primary polydipsia

Excessive fluid intake

How is Na reabsorbed in PCT

70%; Though Na/H (NHE3), Na/Glu, Na/K ATPase, AGII activate NHE3

How is Na reabsorbed in in TAL

20%; NKCC2, paracellular, ADH activate NKCC2

How is Na reabsorbed in DT

6%; Na/Cl cotransporter (NCC) ← AGII can activate

How is Na reabsorbed in CD

ENaC, Na/K ATPase ← Both activated by Aldosterone, ANP decrease ENaC

What is the relationship between GFR and Na

Increase GFR = Increase Na

What is FENa

Fraction of Na → Determines cause of AKI ; FENa = (Urine Sodium × Serum Creatinine) / (Serum Sodium × Urine Creatinine) × 100

What are stimuli for renin release

AA has decreased pressure, stimulation of sympathetic nerve giber on B1 receptor, decreased fluid to macula densa

Action of AGII

Stimulate aldosterone release, thirst and vasopressin release, blood constriction, Na reabsorption at PCT

What is action of aldosterone

Act on principal cell of DT and CD to increase Na reabsorption

What channels does AGII act on in PCT

Na/K ATPase, Na/H (NHE3), Na/HCO3

How is K reabsorbed in different parts of the nephron

PCT (70%) by passive paracellular; Loop of Henle (25%) by NKCC2 and ROMK

What does ROMK do

Secrete K + Reabsorb Ca and Mg

How do aldosterone cause K secretion (DT and CD)

Activate ENaC, Na/K ATPase and ROMK → Na reabsorbed, K secreted

How does ADH cause K secretion (DT and CD)

Activate AQP2 → Na reabsorb, K secreted

What happens when dietary K intake increase

Aldosterone secreted → Acts on ENaC, ROMK and BK → Na reabsorption and K secretion

What happens when dietary K intake decreases

H/K ATP-ase activity increase in intercalated cell of CD → K reabsorption