Potassium Regulation Flashcards
Epinephrine
Lowers serum K+, by uptake into cell of extrarenal tissues even while stimulating K+ excretion by the kidneys
Insulin
Stims Na/K pump causing a flux of K+ into cells and efflux of Na+ from cells. Admin with glucose to treat hyperkalemia
Aldosterone
Increase K+ excretion by kidney; Extrarenal: increase K+ secretion into intestinal fluids and saliva. Enhances acid excretion via production of systemic alkalosis
PT transport
Most of filtered water, Na+, K+, Cl-, HCO3-, Ca+ and Pi are reabsorbed here
Normally all of filtered glucose and amino acids are reabsorbed here
Majority mechanism involves Na/K pump in the basolateral membrane
K+ reabsorption in PT
Driven by lumen-positive transepithlial difference (TEPD)
1) Na+ reabsorbed primarily with HCO3-
2) Cl- gets left behind
3) Negative TEPD
4) Cl- is repelled and reabsorbed
5) Continued NaCl reabsorption drags along water
6) Positive TEPD builds up as Cl- reabsorbs
7) Positive TEPD repels K+
8) K+ reabsorbed paracellularly
LoH transport and medullary recycling
1) K+ secreted into CCD
2) K+ reabsorbed by OMCD
3) K+ floated in interstitium
4) K+ secreted into Later PT/descending thin limbs of LoH
Goal is to increase K+ presence in medulla
Leads to increase in K+ excretion
Principal and Intercalated cells
Principal Cells: Reabsorb Na+ and H2O; secrete K+
a-intercalated cells: Reabsorb K+ and HCO3-; Secrete H+
b-intercalated cells: reabsorb H+ and Cl-; K+ and HCO3-
Factors that stimulate K+ Secretion
- Increased ECF concentration of K+
- Aldosterone
- Increased tubular flow rate
Factors that stimulate K+ reabsorption
- K+ deficiency, low K+ diet, hypokalemia
2. K+ loss thru sever diarrhea
Factors that reg K+ secretion
1) increase activity/insertion of Na/K pump in the basolateral membrane of principal cells
2) Reduced back-leakage of K+ from ICF to renal interstitium
3) Increase synthesis of K-channels and insertion into luminal membrane
4) Increased aldosterone secretion
5) Increased DT flow rate
Increased flow rate enhances K+ secretion
Dilutes the K+ secreted into lumen, thus increasing the K= concentration gradient (K+ is washed away)
Delivers more Na+ to DT for reabsorption, the gradient across the tubular cell rises, K+ secretion is promoted
Decreased flow rate slows K+ secretion
K+ concentrations build up earlier in the tubule, decreasing concentration gradient between cell and tubular fluid, secretion slows
Acute Alkalosis
Alkalosis–acute process that decreases in H+ ion concentration in the extracellular fluid
Alkalemia–physiologically high blood pH
Increased activity of Na/K pump-> increased K+ concentration in interstitium-> increased passive diffusion of K+ into tubule lumen-> increased K+ channels-> increased K+ secretion=hypokalemia
Acute Acidosis
Acidosis–acute process that increases in H+ ion concentration
Acidemia–Physiologically low blood pH
Decreased activity of Na/K pump-> decreased K+ concentration in interstitium-> decreased passive diffusion of K+ into tubule lumen-> decreased K+ channels-> decreased K+ secretion=Hyperkalemia
Acute vs Chronic Acidosis
Chronic acidosis stimulates K+ secretion
Decreased reabsorption of water and solutes by PT by inhibiting Na/K pump-> increases tubular flow to DT and CD-> At same time, RAAS is stimulated due to lack of water reabsorption and subsequent decrease in ECF volume= Changes offset the reabsorptive effects of acute acidosis, and K+ secretion rises
