K+ and Ca2+ Regulation--Muster Flashcards
98% of K+ is located
intracellularly
Insulin’s effect on [K+]serum
decreases [K+]serum by bringing K+ into cells
activates Na+/K+ ATPase
eat food → increase in K+ is coming → let’s make insulin and get ready for it
Catecholemine’s effect on [K+]serum
decreases [K+]serum
β2 receptor stimulation increases activity of Na+/K+ ATPase
Exercise and [K+]serum
increases [K+]serum
muscle cells release measureable amounts of K+ during exercise
insignifigant physiologically
pH effect on K+
**know this**
K+ acts as H+ charge buffer
in acidotic situations:
H+ enters cells to buffer pH
K+ leaves cell, enters serum to buffer charge gradient
acidosis → hyperkalemia
up to 60% buffering of serum pH in this manner
Long-term control of K+ excretion
where
what
how
RAAS system
hyperkalemia → RAAS system activation
SRE activation
increased transcription of ROMK and additional BK channel, moving K+ out into lumen
as well as increase Na+/K+ ATPase and ENaC
occurs in collecting duct: principle cells
K+ reabsorbtion mechanism
how
where
what
in collecting duct intercalated cells
PAY ATTENTION
- to reabsorb K+, we need to secrete H+ via K+/H+ antiporter
- HCO3- must also be made in endothelial cell
- HCO3- carried into interstitium via HCO3-/Cl- antiporter
1˚ means of Ca2+ control
PTH
Ca2+ distribution in blood
40% bound to albumin
10% bound to other things
50% as free ionic Ca2+
iCa2+ (that’s really all we care about)
PTH effect on kidney
distal convoluted tubule
PTH receptor increases calbindin protein
Ca2+ from filtrate binds calbindin
Ca2+ pumped into interstitium via Ca2+ ATPase
PTH mechanisms in Ca2+
bone
release Ca2+ and phosphorus from cortical > trabecular bone
kidney
increase production of activated vitamin D
increase Ca2+ reabsorption
increase renal phosphorus absorption (increase excretion)