Renal Regulation of Potassium Balance Potassium found mostly in intracellular fluid, only 2% in extracellular fluid (closely monitored) 2/3

/3 of body fluid intracellular- collective cytosolic volume of all cells -140-150 mEq/L cytosolic K concentration 1/3 extracellular fluid -Normal: 4 mEq/L K concentration

Resting membrane potentials of nerve and muscle tissues are strongly influenced by the ratio of intracellular to extracellular potassium concentration. Increase extracellular potassium concentration depolarizes the resting membrane potential Decrease extracellular potassium concentration hyperpolarizes cell membranes REGULATION OF POTASSIUM BETWEEN THE INTRACELLULAR AND EXTRACELLULAR COMPARTMENTS Factors that affect extracellular potassium concentration: the total amount of potassium in the body excretion of an amount of urinary potassium equal to the amount of potassium ingested minus the small amounts eliminated in the feces and sweat the distribution of this potassium between the extracellular and intracellular fluid compartments.

RENAL POTASSIUM HANDLING The control of renal function is the major mechanism by which total-body potassium is maintained in balance. Potassium is freely filtered into Bowmans space. 90% is reabsorbed by the proximal tubule and thick ascending limb of the loop of Henle Conserve K - reabsorbed in the distal nephron and medullary collecting duct Body gets rid of K - large amount is secreted in the distal nephron The chief means of regulation lies in control over secretion in parts of the nephron beyond the loop of Henle Proximal Tubule 65% of K reabsorbed unregulated Via: concentration gradient set up when water is reabsorbed & by entrainment with the rapidly reabsorbed water (solvent drag). Thick ascending limb K enter in both membranes actively

1. K pumped into the epithelial cells from the tubular lumen with sodium via Na-K- 2Cl antiporters 2. K from the interstitium via the Na-K-ATPase K exit passively less K than sodium in the lumen, K recycled for multiporter to work

Secretion in the Distal Nephron and its Regulation Principal Cells secrete K - uptake of potassium from the interstitium via the Na-K-ATPase

ROMK (Renal outer medulla) BK (big) Low dietary loads of potassium, there is virtually no secretion on both channels Normal K load - ROMK channels are moved to the luminal membrane and secrete potassium. BK channels-close High excretion rate: both types of channel are present in the luminal membrane secreting potassium

Intercalated Cells (type A)- reabsorb K- reabsorb potassium via the H-K-ATPase in the luminal membrane, which actively takes up potassiumfrom the lumen and then allows potassium to enter the interstitium across the basolateral membrane via potassium channels

Effects of Diuretics Diuretics are agents that increase urine volume and reduce ECF volume. Effects: Increase Na and H20 excretion Side Effect: Increase K excretion Osmotic Diuresis - high filtration of solute that is not reabsorbed) or treatment with diuretics that block sodium reabsorption in the proximal tubule, loop of Henle, or distal convoluted tubule Potassium reabsorption in the proximal tubule and Henles loop is linked to sodium reabsorption diuretics that act on these sites inhibit sodium and potassium reabsorption Decreased Reabsorption of Na & K volume of fluid flowing to the distal nephron per unit Time increased potassium secretion and, hence, excretion Weak Diuretics K sparing Effects of Acid-Base Changes on Potassium Excretion Alkalosis: hypokalemia (low plasma potassium concentration) Acidosis: hyperkalemia Reason of effects: Elevations and depressions in the extracellular concentration of hydrogen ions lead to a de facto exchange of these ions with cellular cations (K)

Low intracellular pH inhibits pumps including Na-K-ATPase and potassium channel activity; high intracellular pH reverses these effects and relieves this inhibition (effectively stimulating the pump and the potassium channels)