H3i: Outline the effect of diuretics on other solutes
- Diuretics aim to ↑Na+ excretion to ↓ECF
- By altering renal handling of Na+, this will have a knock-on effect on other solutes
K+ Excretion
- Diuretic given proximally to the K+ secretory site (DCT, Collecting Duct)
- By ↑Na+ & H2O loss will ↑tubular flow
- This will ↑K+ secretion
- ↓ECF volume will also stimulate Aldosterone, which promotes K+ excretion
HCO3- Excretion
- CA: ↑HCO3– secretion & inhibition H+ secretion ∴metabolic acidosis
- Loop + thiazide
- ↓ECF volume causes subsequent ↑Na+ reabsorption at PCT
- ↑Na+/H+ antiporter activity causing maximal HCO3– reabsorption at PCT (almost all)
- ↓ECF volume
- ↑Aldosterone
- ↑H+ secretion by Principle Cells
- Because almost all HCO3– is reabsorbed at PCT
- H+ secretion to non-HCO3– buffers → which produces NEW HCO3–
- Overall: METABOLIC ALKALOSIS
- K+ sparing:
- Inhibits Na+ reabsorption
- Creates a -ve lumen voltage
- ∴↓H+ secretion
- METABOLIC ACIDOSIS
Ca2+ & Pi Excretion
- All except K+ sparing alters Ca2+ excretion
PCT
- Na + H2O loss
- ↓solvent drag
- ∴↓Ca2+ reabsorption
- NB: Ca2+ is less soluble in alkaline urine → ∴predisposes to formation of Ca2+ containing stores
Loops
- ↑Ca2+ loss by altering voltage
- Normal LoH voltage is +ve
- Drives Ca2+ paracellularly to Peritubular caps
- ∴loss of +ve lumen voltage = loss of Ca2+ reabsorption
Thiazide
- ↑Ca2+ reabsorption
- Blocking Na/Cl symporter
- ↓intrac Na++
- ↑activity of Ca2+/3Na+ symporter
- NB: Thiazides sometimes used to Tx Ca2+ stones in patients with high Ca2+ urine