Renal IIIb Flashcards
About ___ of total body potassium is located within cells because of the Na-K-ATPase pump
98%
The Na-K-ATPase pump actively transport potassium ___ cells.
into
What can occur because the amount of potassium in the ECF is so small?
even very small changes in potassium into or out of cells can produce large changes in extracellular potassium concentration
EC K+ concentration in humans is….
~3.5-5.7 mM
Why is it important to maintain EC concentration of potassium relatively constant?
because of the role of potassium in nerve and muscle excitability
Extracellular potassium is a function of 2 variables:
- total amount of potassium in the body → function of amount of potassium ingested and excreted
- distribution of potassium between extracellular and intracellular fluid compartments → regulated by renal and non-renal mechanisms
What process regulated the amount of Na in the body?
reabsorptive process
What process regulated the amount of K in the body?
net secretory process
⇡ K+ → ⇡ aldosterone → ⇡ K secretion
Amount of potassium excreted in urine by a normal person eating a typical American diet is…
5-15% of filtered quantity
Reabsorption of potassium by the kidney occurs in….
proximal tubule (65%)
thick ascending limb of the Loop of Henle (25%)
medullary collecting duct (5%)
How is K+ reabsorbed in the proximal tubule?
mostly paracellularly
can be transcellular but the mechanisms hasn’t been established
How is K+ reabsorbed in the thick ascending limb of the Loop of Henle?
via the Na-K-2Cl cotransporter
and paracellular mechanisms
How is K+ reabsorbed in the collecting duct?
in the α-intercalated cells there is a H+-K+-ATPase countertransporter which exchanges H+ with K+
What happens to potassium in the cortical collecting duct?
it is secreted under normal circumstances
___ secrete potassium while ___ reabsorb potassium
Principal cells; α-intercalated
What happens to principal cells in the cortical collecting duct during periods of potassium depletion?
they cease secretion of potassium
What mainly regulates changes in potassium excretion?
the cortical collecting duct
Regulation of K+ secretion by the Cortical Collecting Duct:
- Plasma K+ concentration
- Aldosterone
- Flow of Tubular fluid
- Diuretics
- Acid-base balance
What is the critical event for potassium secretion in cortical collecting duct? What does it do?
active transport of potassium from interstitial fluid across the basolateral membrane into the cell, mediated by the basolateral Na-K-ATPase pumps
it creates a concentration gradient for potassium to diffuse into the lumen
Regulation of K+ secretion by the Cortical Collecting Duct: Plasma K+ concentration
high potassium diet → ⇡ plasma potassium (⇡ amount of K+ in blood) → drives uptake of K+ via Na-K-ATPase → ⇡ K+ in cell → drives K+ into tubular lumen
Regulation of K+ secretion by the Cortical Collecting Duct: Aldosterone
Aldosterone enhances tubular secretion of potassium
How does aldosterone work to enhance tubular secretion of potassium?
Aldosterone secreting cells in the adrenal cortex are sensitive to EC K+ concentration → ⇡ in plasma potassium stimulates aldosterone secretion → stimulates potassium secretion by the principal cells of the cortical collecting duct
Anything with a large impact on aldosterone will….
have an impact on K+ secretion and excretion
Regulation of K+ secretion by the Cortical Collecting Duct: Flow of Tubular Fluid
⇡ flow rate to the cortical collecting duct → ⇡ K+ secretion in the cortical collecting tubule
B/C ⇡ flow rate → tends to dilute K+ concentration in the luminal fluid - enhances K+ gradient for secretion
⇡ Flow rate → ⇡ K+ secretion → ⇡ K+ excretion
⇡ Flow rate → ⇡ Na reabsorbed → ⇡ K+ secretion
Regulation of K+ secretion by the Cortical Collecting Duct: Acid-Base Balance
Alkalosis stimulates Na-K-ATPase activity in the cortical collecting duct → K+ levels ⇡ within the principal cells → secretion via K+ channels into the tubule lumen increases
What happens to K+ in patients suffering from alkalosis induced by vomiting?
there is ⇡ K+ secretion and hence excretion
Regulation of K+ secretion by the Cortical Collecting Duct: Diuretics
diuretics → ⇡ Flow rate → always ⇡ K+ secretion and excretion
Relationship between sodium excretion and potassium secretion mechanisms
changes in Na reabsorption mechanisms are not coupled with K+ secretion mechanisms
Why are changes in Na reabsorption mechanisms are not coupled with K+ secretion mechanisms?
⇡⇣
high sodium diet → ⇡ ECF → ⇣ sympathetic activity and renal Ang II → ⇣ aldosterone secretion → ⇣ K+ secretion at the cortical collecting ducts
high sodium diet → ⇡ ECF → ⇡ GFR → ⇡ fluid delivery to cortical collecting ducts → ⇡ K+ secretion at the cortical collecting ducts
overall effect is that K+ secretion is unchanged
Renal Calcium regulation
calcium is reabsorbed paracellularly down its electrochemical gradient in the thick ascending limb of the loop of henle
Ca is reabsorbed via calcium channels in the distal tubule
What occurs in response to hypocalcemia (⇣ Ca in blood)?
Parathyroid hormone (PTH; released by parathyroid gland) is released and acts to increase calcium reabsorption at the level of the distal tubule
Renal Phosphate Regulation
Phosphate that is not bound to plasma proteins is filtered across glomerular capillaries
85% of phosphate is reabsorbed in the proximal tubules
15% is excreted
How does PTH regulate reabsorption of phosphate in the proximal tubule?
by inhibiting Na+-phosphate cotransport, thereby decreasing the phosphate reabsorption
PTH
increases Ca reabsorption in the distal tubule
decreases Phosphate reabsorption in proximal tubule (inhibits phosphate reabsorption)
Renal Mg reabsorption
95% reabsorption of Mg
30% in proximal tubules
60% in thick ascending limb of loop of henle
5% in distal tubule
reabsorbed paracellularly down its electrochemical gradient in the thick ascending limb of the loop of henle
Proteins and Peptides
binding of proteins to specific receptors then endocytosis
Intracellular vesicles merge with lysosomes whose enzymes degrade protein to low molecular weight fragments (amino acids)
End products the exit the cells across the basolateral membrane into the interstitial fluid from which they enter peritubular capillaries
Active Proximal Tubule Secretion of Organic Anions
Active secretory pathway for organic anions in proximal tubule has relatively low specificity → single kind of transporter is responsible for secretion of all organic anions
Active Proximal Tubule Secretion of Organic Anions: PAH
PAH is actively transported into proximal tubular cell across the basolateral membrane → the resulting intracellular concentration then provides the gradient for facilitated diffusion of PAH across the luminal membrane into the tubular lumen
Renal handling of Organic cations
transported across the basolateral membrane by facilitated diffusion mechanism → drive by negative potential difference across the basolateral membrane
transport across the luminal membrane is mediated by OC+-H+ antiporter → antiporter is nonspecific and other organic cations can compete with it
