Tubular Secretion Flashcards
Probenecid
Inhibits organic anion secretion
Organic Anion Secretion
OA-s cross the basolateral membrane via a-ketoglutarate antiporters (OATS) ; crosses the apical membrane via MRP2 or OAT4
*a-ketoglutarate enters cell via NaDC symporter
Organic Cation Secretion
OC+s enter the cell via passive diffusion and OCTs; leave cell in exchange for 2H+ by OCTNs or MDR1
*Are able to enter cell due to electrical gradient
ERPF
Effective Renal Plasma Flow
Measured by Cpah, this is 10% less than the actual renal plasma flow
Extraction Fraction
E= A-V/A
RPF equation
RPF= Cpah/Epah
Uric Acid Flux
Net direction is reabsorption; undergoes this in the early proximal tubule and is secreted in the late proximal tubule
Four factors of hyperuricemia in gout
- Decreased filtration rate
- Increased reabsorption rate
- Decreased secretion rate
- Increased production
K+ transport
Proximal tubule: Area where most is reabsorbed; about 2/3 AT ANY METABOLIC STATE
Collecting duct: Under the influence of aldosterone, principal cells will secrete more indirectly thru increased activity of Na+/K+ ATPase
Low K+ intake effects on distal tubule
Decreased luminal permeability and increased TF flow will ultimately have no effect on K+ secretion
*Increased TF flow will nomally increase secretion
Mechanisms of K+ transport
- Increased TF
- K+ conc. gradients (Increased [K+] ICF => increased secretion)
- Electrical gradient (Na+ reabsorption => more K+ secretion)
- Aldosterone
- Alkalosis (Increases ICF [K+]
- CHRONIC Acidosis (Increased NaCl reabsorption)
Aspirin Poisoning
Alkalosis causes the ionization of weak acids, trapping the acetylsalicylate in the urine
=> Increased excretion
K+ intake
Is equal to K+ output; kidneys are primary regulators of [K+]
