Lecture 11: K+ Regulation Flashcards
Hyper/hypokalemia
High or low EXTRACELLULAR K+
Where does renal K+ regulation primarily occur?
In the cortical CD (control of secretion); normally, most K+ is reabsorbed.
How is K+ secreted in the cortical collecting ducts?
Basolateral: Na+/K+ ATPase brings K+ into cell
Apical: K+ channels excrete K+, assoc. w/ Na+ reabsorption
Angiotensin II response to acute low MAP
Low Ang II preferentially constricts efferent arterioles, lowering RBF to maintain GFR e.g. dehydration
Angiotensin II response to pathologic low MAP
High Angiotensin II constricts aff. + efferent arterioles; RAAS is maxed out, lowering RBF and GFR. The decreased peritubular cap. P increases H2O and ion reabsorption
3 stimulators of cellular K+ uptake
- Increased plasma [K+] via Na+/K+ ATPase
2 and 3. Insulin and epi both stim. K+ uptake via Na+/K+ ATPase
Effects of osmolarity on K+ levels
HyperOsm.: cell shrinkage -> increased IC [K+] -> increased K+ exit -> hyperkalemia
HypoOsm.: cell swelling -> lower IC [K+] -> less K+ exit -> hypokalemia
Acid/base causes for K+ shifts
Works due to proton in/K+ out exchange (sequence of steps)
Acidosis -> hyper-K
Alkalosis -> hypo-K
Renal K+ processing by tubular segment
PT: reabsorption secondary to H2O
Thick ascend. limb: NKCC reabsorption
DT/CD: varied secretion/resorption; principal cells secrete, α intercalated cells reabsorb K+
Distal tubule/collecting duct fine tuning of K+
Low K+ intake: α intercalated cells reabsorb K+ (H+ exchange
High K+ intake: principal cells secrete K+ through apical channels (basolateral Na+/K+ ATPase from blood)
RAAS and aldosterone effect on K+
Aldosterone increases K+ secretion
- Electrochem. gradient shift: increased ENaC, Na/K ATPase
- Increased permeability of apical K+ channels
- Activation + synthesis of transporters (short + long term)
Apical K+ channels
- ROMK (Renal Outer Medullary K Channel
- BK (Big capacity K channel)
How does tubular fluid flow affect K+ excretion?
Increased flow increases secretion due to concentration gradient
1. More Na+ delivery -> depolarization stimulating Na/K ATPase
2. Cilia deflection raises IC Ca2+ activating BKs -> more apical K+ permeability
Aldosterone paradox
Decreased ECF -> AII leads to no net change in K+ secretion
How does acidosis affect K+ secretion acutely and chronically?
Acute: acid directly inhibs apical/basolateral channels, reducing K+ secretion
Chronic acid: increased distal flow + high aldosterone can increase K+ secretion
How does alkalosis affect K+ secretion?
Alkalosis can directly stimulate K+ secretion
Difference between K+ wasting and sparing diuretics
K+ wasting diuretics work upstream of the CD (loop, thiazides)
K+ sparing block Na+ reabsorption at principal cells (CDs)
