K+ and Ca2+ Regulation

Question 1

What percentage of K+ filtered load is reabsorbed in the proximal tubule by tight junctions?

Answer 1

55-65%

Question 2

How much of the filtered K+ is reabsorbed by the time it reaches the principal cells in the distal convoluted tubule and collecting duct?

Answer 2

80-90%!

Question 3

What will the principal cells do with K+ during a high K+ diet?

Answer 3

they will secrete it

intracellular K+ concentration increases in ALL cells with high K+ diet, since the extra dietary K_ moves into all cells iva Na/K ATPase pumps

THe prinicpal cell then secretes the K+ back into the lumen to achieve K+ homeostasis, such that K excretion rate is higher than the filtered load of K

Question 4

What are the two channels that are increased in the principal cells during periods of high K+ concentration?

Answer 4

the renal outer medullary K channels (ROMK) (because you have high aldosterone in response to high K+)
the large conductance or big K+ channel (BK)

Question 5

What happens in the principal cell with a low K+ diet?

Answer 5

the BK channels aren’t expressed and ROMK channels are decreased

Question 6

What kind of cell in the distal tubule and collecting duct will actively reabsorb K during a low K+ diet?

Answer 6

the alpha or type A intercalated cell

Question 7

What will the K+ excretion rate be when the type A intercalated cells are doing their thing?

Answer 7

only 1% of the K+ diltered load

Question 8

Why is hypokalemia often accompanied by a loss of H+ (alkalosis)?

Answer 8

The type A intercalated cells use a K+/H+ ATPase to resabsorb the K+, so more H+ gets pumped into the lumen and excreted, thus leading to low H+ and alkalosis

Question 9

Once the K+ is brought in to the alpha-intercalated cell, how does it leave the cell and enter the extracellular fluid/plasma?

Answer 9

Just a plain old K+ channel - it diffuses down it’s concentration gradietn

Question 10

What is the major hormone that controls Ca2+ excretion?

Answer 10

parathyroid hormone (PTH)

Question 11

When is PTH released?

Answer 11

In response to decreased free Ca2+ in the plasma - sensed by the calcium-sensing receptor (a GPCR) on the surface of the parathyroid cell

Question 12

What is the major way that PTH increases Ca2+ concentration?

Answer 12

It’s through bone -

it turns off the osteoblasts and turns on the osteoclasts, so you get resorption of bone, releasing Ca2+ and phosphate

Question 13

What is PTH’s effect on vitamin D?

Answer 13

It stimulates renal activation of vitamin D, which leads to increased intestinal Ca2+ absorption (since you need vit D to absorb it)

Question 14

How does PTH directly increase Ca2+ reabsorbtion in the kidney?

Answer 14

When the PTH receptor is activated, you get increased luminal Ca2+ channel expression

Question 15

Once the Ca2+ is brought into the epithelial cell int he distal convoluted tubule, how does it get into the extracellular fluid and plasma?

Answer 15

via the Ca2_ ATPase
and
via secondary active transport via the Na+/Ca2+ antiporter

Question 16

Why do you get bone resorptoin and bone weakness in kidney disease? What is this called?

Answer 16

renal osteodystrophy

without good kidneys, you don’t get activation of vitamin D (no calcitrol)

since you don’t have calcitrol, you have decreased Ca2_ intestinal absorption. This means you have a decrease in free plasma Ca2+ concentration, which triggers an increase in PTH release. The PTH shuts down osteoblasts and turns on osteoclasts, so you get bone resorption and weak bones