Potassium regulation
amount in body
ECF: only 2% of total body K+
(regulated at 4.2mEq/L, usu. +/- 0.3mEq/L)
ICF: 98% of total body K+
intake
High daily intake: 50 - 200mEq/day
Strict regulation of ECF concentration otherwise hyper/hypokalemia
Regulation primarily by
1) KIDNEY excretion
(rate of filtration, reabsorption, secretion)
2) redistribution between ECF and ICF
(first line defense)
Factors that alter K+ distribution between ICF and ECF
Insulin: uptake into cell (DM)
Aldosterone: uptake into cell (Conn's sx and Addison's dx)
Beta2-adrenergic: uptake into cell (beta blockers in treating hypertension)
Metabolic acidosis: increase ECF K+ due to H+ on Na-K ATPase pump--> decreased uptake of K+
Cell lysis: increase ECF K+ (MS injury/ RBC lysis)
Strenuous exercise: increase ECF K+ due to release from skeletal MS
Increased ECF osmolarity: increase ECF K+ due to osmotic flow --> K+ diffuse along gradient to ECF
Renal K+ excretion
click to edit
Daily variations takes place here
Reabsorbed at Proximal tubule and thick ascending limb of loop of Henle: cotransported with Na+ and Cl-
Reabsorbed or secreted at Distal and Collecting tubule (principle cells of late Distal and cortical Collecting tubules):
Secretion: Na/K ATPase pump at basolateral, ROMK passive diffusion at luminal. Reabsorption: H/K ATPase at luminal, diffuse at basolateral
Stimulate K secretion by principle cells: 1) increased ECF [K] (Na/K ATPase stimulated; increased conc gradient to prevent backflow; stimulate aldosterone secretion!) 2) increased aldosterone (Na/K ATPase and permeability) 3) increased tubular flow rate
Decrease K secretion: acute acidosis (Na/K ATPase pump) BUT chronic acidosis leads to more K secretion b/c proximal tubular NaCl and water reabsorption is inhibited! more distal volume stimulates K secretion
Na vs K
K secretion when Na intake changes
The effect of increased tubular flow rate is especially important in helping to preserve normal
potassium excretion during changes in sodium intake. For example, with a high sodium intake, there is
decreased aldosterone secretion, which by itself would tend to decrease the rate of potassium
secretion and, therefore, reduce urinary excretion of potassium. However, the high distal tubular flow
rate that occurs with a high sodium intake tends to increase potassium secretion. Therefore, the two effects of high sodium intake, decreased
aldosterone secretion and the high tubular flow rate, counterbalance each other, so there is little
change in potassium excretion.
K and Na in DIET
For most of human history, the typical diet has been one that is low in sodium and high in potassium
content, compared with the typical modern diet. This is
due to their consumption of a diet containing large amounts of fruits and vegetables and no processed
foods. Populations consuming this type of diet typically do not experience age-related increases in
blood pressure and cardiovascular diseases. Experimental and clinical studies have shown that the combination of high sodium and low potassium
intake increases the risk for hypertension and associated cardiovascular and kidney diseases. A diet
rich in potassium, however, seems to protect against the adverse effects of a high-sodium diet