Lecture 19: Renal Regulation Of Ion Concentrations Flashcards
Describe extracellular potassium
- Normally precisely regulated at 4.2 mEq/L (±0.3 mEq/L).
- An increase of 3 to 4 mEq/L can lead to cardiac arrhythmias.
- Higher concentrations can lead to cardiac arrest or fibrillation.
- Extracellular fluid contains 2% of total body potassium.
- Note that intake of potassium from a single meal can be as high as 50 mEq.
- Kidneys must adjust potassium excretion rapidly and precisely in response to wide variations in intake.
- Mainly involves distal and collecting tubules.
Describe intracellular potassium
- What is the normal intracellular concentration of potassium ion?
- 140 mEQ/L
- Total amount of potassium in body compartments:
- Extracellular = 4.2 mEq/L x 14 L = 59 mEq
- Intracellular = 140 mEq/L x 28 L = 3920 mEq
- Refer to Figure 29-1.
Describe Major factors responsible for potassium excretion
- Direct influence on distal renal tubules and collecting ducts via increase in extracellular potassium ion concentration.
- Effect of aldosterone secretion on potassium excretion:
- Increase in extracellular potassium stimulates increase in aldosterone secretion.
What are the main sites of potassium reabsorption and secretion?
- Reabsorption:
- Proximal tubule
- Ascending limb of Henle
- Secretion:
- Late tubule
- Collecting duct
- See Slides 9-10
See slide 11 for Mechanisms of potassium secretion and sodium reabsorption and secretion by principal cells.
Note that potassium secretion by principal cells is stimulated by potassium concentration and aldosterone.
Describe the Effect of plasma aldosterone concentration and extracellular potassium ion concentration on rate of urinary potassium excretion.
See Slide 12
Describe the Effect of extracellular fluid potassium ion concentration on plasma aldosterone concentrations.
See Slide 13
Note that small changes in potassium concentration cause large changes in aldosterone secretion by adrenals.
Describe Mechanisms by which high potassium intake raises potassium excretion.
See Slide 14
- Direct influence on kidneys via high potassium concentration.
- Indirect via aldosterone secretion.
Describe the Effect of large changes in potassium intake on extracellular fluid potassium concentration under normal conditions.
See Slide 15
- Blockage of aldosterone system impairs regulation of potassium concentration.
Describe the Relationship between flow rate in cortical collecting tubules and potassium secretion and the effect of changes in potassium intake.
See Slide 16
- Conditions that cause an increase in tubular flow rate:
- Volume expansion
- High sodium intake
- -Note: High K+ diet greatly enhances effect of increased tubular flow rate to increase K+ secretion
- Some diuretics
– Note that high potassium intake greatly increases the potassium secretion rate even at low tubular flow rates.
Describe the Effect of high sodium intake on renal excretion of potassium
See slide 18
- Note that increased sodium intake decreases aldosterone secretion and, therefore, potassium excretion.
- However, Increased sodium intake also increases GFR and decreases proximal tubular reabsorption of sodium. This leads to an increase in distal tubular flow rate and increase in potassium excretion.
- Therefore, High sodium diet leads to little change in potassium excretion.
- Compare a high sodium/low potassium diet with a low sodium/high potassium diet. (See page 395)
Describe parathyroid hormone’s (PTH) effect on maintaining a constant extracellular concentration of calcium
- About 50% of total plasma calcium is in the ionized form.
- Ionized has biological activity at cell membranes.
- Changes in plasma pH on calcium binding:
- Acidosis:
- Less calcium is bound to the plasma proteins
- Alkalosis:
- More calcium is bound to the plasma proteins.
- A large amount of calcium excretion occurs in the feces; therefore, GI tract is important in calcium homeostasis.
- Almost all the calcium in the body is stored in the bone.
- PTH is one of the most important regulators of bone uptake and release of calcium.
- Parathyroid glands are directly stimulated by low calcium levels.
- Increase secretion of PTH.
Describe calcium reabsorption with regards to the effects of PTH and in the proximal tubule
- PTH effects (See Figure 29-11):
- Stimulates bone reabsorption
- Stimulates activation of vitamin D
- Note that calcium is filtered and reabsorbed but not secreted.
- Indirectly increases tubular calcium reabsorption
- Reabsorption in proximal tubule:
- About 99% of filtered calcium is reabsorbed:
- About 65% is reabsorbed in the proximal tubule mostly through paracellular route
- About 20% is reabsorbed in the proximal tubule mostly through transcellular route:
- – Electrochemical gradient
- – Basolateral calcium-ATPase and sodium-calcium countertransporter
Describe calcium reabsorption in the loop of henle
- Restricted to thick ascending limb
- 50% through paracellular route
- Passive diffusion and slight positive charge of tubular lumen
- 50% via transcellular route stimulated by PTH
Describe calcium reabsorption in the distal tubule, and factors that regulate tubular calcium reabsorption
- Reabsorption in distal tubule:
- Almost entirely via active transport:
- Calcium-ATPase pump in basolateral membrane
- Stimulated by PTH
- Factors that regulate tubular calcium reabsorption:
- ↑ levels PTH (Decreases calcium excretion)
- ↑ Plasma concentration of phosphate (Decreases calcium excretion)
- ↑ Metabolic alkalosis (Decreases calcium excretion)
- Refer to Table 30-2
- See Figures 30-11 and 30-12
- See slides 25-26
