In addition, when H+ is expelled from the cell (by H+ATP-ase), cations—in this case potassium—are taken up by the cell in order to maintain electroneutrality (but not through direct exchange as with the H+-K+ATPase). In order to correct the pH during alkalosis, these cells will use these mechanisms to reabsorb great amounts of H+, which will concomitantly increase their intracellular concentrations of potassium. This concentration gradient drives potassium to be secreted across the apical surface of the cell into the tubular lumen through potassium channels (this facilitated diffusion occurs in both Type B intercalated cells and Principal cells in the collecting duct).2) Metabolic alkalosis is often present in states of volume depletion, such as vomiting, so potassium is also lost via aldosterone-mediated mechanisms.3) During metabolic alkalosis, the acute rise of plasma HCO3− concentration (caused by vomiting, for example) will exceed the capacity of the renal proximal tubule to reabsorb this anion, and potassium will be excreted as an obligate cation partner to the bicarbonate. Disease states that lead to abnormally high aldosterone levels can cause hypertension and excessive urinary losses of potassium. These include renal artery stenosis and tumors (generally nonmalignant) of the adrenal glands, e.g., Conns syndrome (primary hyperaldosteronism). Cushings syndrome can also lead to hypokalemia due to excess cortisol binding the Na+/K+ pump and acting like aldosterone. Hypertension and hypokalemia can also be seen with a deficiency of the 11-beta-hydroxysteroid dehydrogenase type 2 enzyme which allows cortisols to stimulate aldosterone receptors.
Oral potassium supplementation
Mild hypokalemia (>3.0 mEq/L) may be treated by eating potassium-containing foods or by taking potassium chloride supplements in a tablet or syrup form (by mouth supplements). Foods rich in potassium include dried fruits (particularly dried figs), nuts, bran cereals and wheat germ, lima beans, molasses, leafy green vegetables, broccoli, winter squash, beets, carrots, cauliflower, potatoes, avocados, tomatoes, coconut water, citrus fruits (particularly oranges), cantaloupe, kiwis, mangoes, bananas, and red meats.Eating potassium-rich foods may not be sufficient for correcting low potassium; potassium supplements may be recommended. Potassium contained in foods is almost entirely coupled with phosphate and is thus ineffective in correcting hypokalemia associated with hypochloremia that may occur due to vomiting, diuretic therapy, or nasogastric drainage. Additionally, replacing potassium solely through diet may be costly and result in weight gain due to potentially large amounts of food needed. An effort should also be made to limit dietary sodium intake due to an inverse relationship with serum potassium. Increasing magnesium intake may also be beneficial for similar physiological reasons.Potassium chloride supplements by mouth have the advantage of containing precise quantities of potassium, but the disadvantages of a taste which may be unpleasant, and the potential for side-effects including nausea and abdominal discomfort. Potassium bicarbonate is preferred when correcting hypokalemia associated with metabolic acidosis. Intravenous potassium replacement
Severe hypokalemia (<3.0 mEq/L) may require intravenous supplementation. Typically, a saline solution is used, with 20–40 meq/L KCl per liter over 3–4 hours.