Electrolyte and pH balance (Ch. 26 Part II) Flashcards
Na+ Balance and aldosterone
Body tries to hang onto Na+, reabsorbs it in kidneys and that helps us reabsorb water too 65% in PCT (majority of reabsorption occurs in PCT, filtrate volume decreases a lot) 25% in loops of Henle,
High [aldosterone]: The rest (10%) is absorbed in the DCT & CD,
Low [aldosterone]: Na+ is not actively reabsorbed- lost to urine, water follows
aldosterone’s effects on K+ balance
since Na+ gets reabsorbed in higher amounts with aldosterone due to more Na-K pumps, K+ goes the other way and we urinate it out
ANP’s effects at kidney
opposite of aldosterone, increases urine output, decreases BP because it increases urine output to bring BV down
eliminates sodium from the body, water follows
[effect on GFR as it relates to contractile activity of glomerular mesangial cells]
estrogen
- High [aldosterone]:
- The rest (10%) is absorbed in the DCT & CD
- Low [aldosterone]:
- Na+ is not actively reabsorbed- lost to urine, water follows
Progesterone
- Progesterone decreases Na+ reabsorption (blocks aldosterone)•
- Promotes Na+ and H2O loss
K+’s importance in APs and RMP
affects RMP and generation APs in neurons and muscle cells (so does sodium and calcium)
hyperkalemia
high ECF [K+] causes depolarization & hyperexcitability, RMP closer to threshold potential, too many APs quickly fired during period of hyperexcitability, so reduced excitability follows and can lead to cardiac arrhythmia → arrest
reversal potential review
charge difference at which you start reversing the flow of potassium because the cell is so negative inside that for every K+ that exits, another is pulled in (-90 for K+, +55 for Na+)
hypokalemia
very dangerous because can easily lead to unresponsiveness and sudden cardiac arrest
Regulation of K+ Balance
K+ balance is controlled in cortical collecting ducts by regulating amount secreted into filtrate
- Most important factor affecting K+ secretion is its concentration in ECF, which is determined by diet
- K+ controls its own ECF concentration via feedback regulation of aldosterone release
how can acidosis lead to hyperkalemia
lots of hydrogen ions moving into cell, H+ wants to bind to P-, potassium leaves cell to balance charge, hyperkalemia
PTH (parathyroid hormone)
released from parathyroid gland in response to Ca2+ dropping, because we need to get more Ca2+ into blood
3 ways PTH increases Ca2+ in blood
increase osteoclast activity in bone to cause Ca2+ and PO43- release into blood, increase Ca2+ reabsorption in kidney tubule, higher activation of vitamin D by kidney which increases Ca2+ absorption from food in small intestine
where each buffer plays its biggest role
understand bicarbonate buffer system intimately