L10 Potassium homeostasis: renal contributions Flashcards
Cell functions K+ is Critical for?
regulation of cell volume
regulation of intracellular pH
maintaining potential difference across cell membrane
Hyperkalemia’s Effect on ECG?
Increases T Waves
Further increases prolong PR interval, depress ST segment, and lengthen QRS
As plasma [K+] approaches 10 mEq/L, P wave disappears, QRS interval broadens, the ECG appears as a sine wave(ventricular fibrillation)
Hypokalemia’s Effect on ECG?
prolongs the QT interval
Inverts the T wave
Lowers the ST segment
Factors that Alter Plasma [K+]
- Food intake
- Acid-Base Balance (Metabolic Acidosis (increased [H+]) => movement of H+ into cells and reciprocal movement of K+ out of cells ( Increased Plasma [K+])
- Plasma Osmolality
- Cell Lysis and Exercise (Increase Plasma [K+])
Kidney is primarily responsible for maintaining total body K+ content (takes hours). As such K+ concentration is initially buffered by the movement of K+ into/out of _________________
Internal K+ Balance is regulated by:
- ________________________
- ________________________
- ________________________
Kidney is primarily responsible for maintaining total body K+ content (takes hours). As such K+ concentration is initially buffered by the movement of K+ into/out of skeletal muscle
Internal K+ Balance is regulated by:
- Catecholamines (epinephrine): activates adrenergic (alpha= release K+, Beta = uptake) receptors on target cells (Minutes)
- Insulin: Stimulates uptake of K+ into cells (Minutes)
- Aldosterone: Stimulates uptake of K+ into cells and urinary K+ secretion (~1hr)
Excretion of K by the kidneys is regulated by?
- ________________________
- ________________________
- ________________________
Excretion of K by the kidneys is regulated by:
- Plasma [K]
- Aldosterone (Steroid hormone) passes through the membrane of principal cells & binds mineralocorticoid receptors=> bound receptor acts as transcription factor increasing: Na/K+ ATPase on the basolateral surface, Increased K+ channels on APical relative to basolateral => driving secretion of K+ from body
- ADH: Net K secretion is not affected
What cells are primarily responsible for regulating K+ excretion?
Regulation of K+ excretion is achieved mainly by alterations in K +secretion by principal cells of late distal tubule and collecting duct cells
The proximal tubule reabsorbs _____% of the filtered K+
K+ reabsorption in PCT is primarily due to _________ via solvent drag but also due to a shift in __________________
The proximal tubule reabsorbs ~67% of the filtered K+
K+ reabsorption in PCT is primarily due to paracellular movement via solvent drag but also due to a shift in transepithelial voltage
The TAL reabsorbs about ____% of filtered K+
K+ reabsorption in TAL due to both transcellular movement via ___________ and paracellular movement due to _____________ generated by apical K+ channels
Thick ascending limb DOES NOT REABSORB WATER, so no _________
The TAL reabsorbs about 20% of filtered K+
K+ reabsorption in TAL due to both transcellular movement (by NKCC2) and paracellular movement due to the lumen positive voltage generated by apical K+ channels
Thick ascending limb DOES NOT REABSORB WATER, so no solvent drag
The DCT and Ccollecting duct can reabsorb K+ (_____________) or secrete K+ (____________)
- ____________cells reabsorb K+ via H+/K+ ATPase transporter
- ____________cells secrete K+ via K+ channels (ROMK channels)
Principle Cell
- _____________ is present throughout DCT and Collecting Duct
- _____________ begins in the DCT2 w/ combined presence of ROMK (K+ channel), ENaC, and Aldosterone Sensitivity.
Intercollated Type A
- No ______________ on basolateral side! Energy required for transport derived from _________________________________________
The DCT and Ccollecting duct can reabsorb K+ (Type A Intercalated Cells) or secrete K+ (_Principal cells)
- Intercalated cells reabsorb K+ via H+/K+ ATPase transporter
- Principal cells secrete K+ via K+ channels (aka ROMK channels)
Principle Cell
- Electroneutral K+/Cl- co-transport is present throughout DCT and Collecting Duct
- Electrogenic-Mediated K+ transport begins in the DCT2 w/ combined presence of ROMK (K+ channel), ENaC, and Aldosterone Sensitivity.
Intercollated Type A
- No Na+/K+ ATPase pumps on basolateral side!! Energy required for transport derived from H+ gradient generated by H+ ATPases on the apical side
__________ is responsible for K+ secretion in the initial collecting duct and cortical collecting duct
Principal cell is responsible for K+ secretion in initial collecting duct and cortical collecting duct
Factors that influence K+ secretion by the cortical collecting ducts?
- Plasma [K]
- Aldosterone
- Antidiuretic hormone (Minor Response- Cancels Out): ADH increases K secretion which compensates for the decreased tubular fluid flow rates they cause
Thresholds of Hyperkalemia/Hypokalemia?
ECF [K+] > ______ mEq/L constitutes hyperkalemia
ECF [K+] < _____ mEq/L constitutes hypokalemia
ECF [K+] > 5.0 mEq/L constitutes hyperkalemia
ECF [K+] < 3.5 mEq/L constitutes hypokalemia
Role of Plasma [K+] in K+ secretion? (5 Mechanisms)
ECF [K+] > 5.0 mEq/L constitutes hyperkalemia and stimulates secretion of K+ within minutes via several mechanisms:
- Stimulates Na+-K+-ATPase resulting in increased K+ uptake across the basolateral membrane => increases the electrochemical driving force for exit of K+ across the apical membrane
- Increases permeability of the apical membrane to K+
- Increases secretion of aldosterone by adrenal glands
- Increases flow rate of tubular fluid which stimulates secretion of K+
An ECF [K+] < 3.5 mEq/L constitutes hypokalemia and results in opposite effects to those outlined above
MOA/Indication for Spironolactone?
The action of aldosterone blocked by Spironolactone, a potassium-sparing diuretic (water pill), used to treat and/or prevent oedema and hypokalemia
