Lecture 19: Regulating Renal Ion [ ] Flashcards
What is normal extracellular [ ] of K+ ion?
Normal= 4.2 mEq/L
What is the clinical significance of excess extracellular K+?
Cardiac arrhythmias, cardiac arrest, or fibrillation.
Why must the kidneys be able to rapidly adjust extracellular K+ [ ]?
Must be maintained around 4-5 d/t risk of cardiac arrhythmias, arrest, fibrillation.
Must be maintained b/c of the varied intake in a diet to keep balanced. [take in alot in diet vs low [ ] extracellular.
What is the overall effect of aldosterone secretion on K+ excretion?
Increase in extracellular K+ stimulates increase in aldosterone secretion= more K+ excretion
Fig 30-4: aldosterone increases = K+ excretion increases
Aldosterone and extracellular [K+] factors in K+ excretion
What part of the renal tubule is responsible for K+ reabsorption and what part is responsible for K+ secretion?
Reabsorption: proximal tubule and ascending limb of henle
Secretion: late tubule and collecting duct
Describe the mechanism by which principal cells secrete K+?
Na+ is pumped into the interstitial
K+ is pumped out of cell into tubular lumen.
This is stimulated by K+ and aldosterone.
Maybe look up more?
What factors stimulate principal cells to secrete k+?
Aldosterone and extracellular [K+] factors in K+ excretion
Describe the relationship btw tubular flow rate and K+ secretion:
High K+ diet greatly enhances effect of increases tubular flow rate to increase K+ secretion.
High K+ intake greatly increases the K+ secretion rate even at low tubular flow rates.
Conditions that cause increase tubular flow rate: volume expansion, some diuretics, and high Na+ diet
Describe and explain why high Na intake has little effect on K+ excretion.
High Na+ intake decreases aldosterone secretion, which decreases K+ excretion.
Can eliminate Na+ w/o eliminating K+, BUT
This increases GFR and decreases proximal tubular reabsorption of Na+, leading to increase in distal tubular flow rate and increase in K+ excretion
Its a wash
How does plasma pH effect the amt. of plasma ca++ bound to plasma proteins?
Acidosis: LESS Ca++ is bound to plasma proteins.
Alkalosis: MORE Ca++ is bound to plasma proteins.
List the effects of PTH(3):
- Stimulates bone reabsorption
- Stimulates activation of Vit D
- Indirectly increases tubular Ca++ resorption
PTH is important regulator of bone uptake and release of Ca++
How much filtered Ca++ is reabsorbed, and where in the kidney tubule does this occur?
99%:
- 65% in proximal tubule through paracellular route.
- 20% in proximal tubule through transcellular route
Ca++ is filtered and reabsorbed but not SECRETED
Restricted to thick ascending limb
Distal tubule
List the factors that decrease Ca++ reabsorption:
Factors that decrease Ca++ excretion:
- increases levels PTH
- increase plasma [ ] of phosphate
- increase metabolic alkalosis
Look at fig 30-11: the opposite decreases Ca+ REABSORPTION:
- decrease levels of PTH
- decrease plasma [ ] of phosphate
- decrease metabolic alkalosis
What effects do insulin and catecholamines have on extracellular K+ levels?
Insulin: simulates K+ uptake by cells
Catecholamines: ß-adrenergic stimulation (epinephrine)- stimulates K+ uptake by cells.
–ß-adrenergic receptor blockers->hyperkalemia
What’re the relationships of Conn’s syndrome and addisons Dz to aldosterone secretion and K+ levels?
Conn’s: excess secretion of aldosterone (hypokalemia)
Addisons: deficiency in aldosterone secretion (hyperkalemia)