INTERCOMPARTMENTAL SHIFTS OF POTASSIUM
Intercompartmental shifts of potassium are known to occur following changes in extracellular pH , circulating insulin levels, circulating catecholamine activity, plasma osmolality, and pos-sibly hypothermia. Insulin and catecholamines are known to directly affect Na +–K+-ATPase activity and decrease plasma [K+]. Exercise can also tran-siently increase plasma [K+] as a result of the release of K+ by muscle cells; the increase in plasma [K+] (0.3–2 mEq/L) is proportionate to the intensity and duration of muscle activity. Intercompartmental potassium shifts are also thought to be responsible for changes in plasma [K+] in syndromes of periodic paralysis .
Because the ICF may buffer up to 60% of an acid load , changes in extracellu-lar hydrogen ion concentration (pH) directly affect extracellular [K+]. In the setting of acidosis, extra-cellular hydrogen ions enter cells, displacing intra-cellular potassium ions; the resultant movement of potassium ions out of cells maintains electrical bal-ance but increases extracellular and plasma [K+]. Conversely, during alkalosis, extracellular potas-sium ions move into cells to balance the movement of hydrogen ions out of cells; as a result, plasma [K+] decreases. Although the relationship is variable, a useful rule of thumb is that plasma potassium con-centration changes approximately 0.6 mEq/L per 0.1 unit change in arterial pH (range 0.2–1.2 mEq/L per 0.1 unit).
Changes in circulating insulin levels can directly alter plasma [K+] independent of that hor-mone’s effect on glucose transport. Insulin enhances the activity of membrane-bound Na+–K+-ATPase, increasing cellular uptake of potassium in the liver and in skeletal muscle, and insulin secretion may play an important role in the basal control of plasma potassium concentration and in the physiological response to increased potassium loads.
Sympathetic stimulation also increases intra-cellular uptake of potassium by enhancing Na+–K+-ATPase activity. This effect is mediated through activation of β2-adrenergic receptors. In contrast, α-adrenergic activity may impair the intracellularmovement of K+. Plasma [K+] often decreases fol-lowing the administration of β2-adrenergic agonists as a result of uptake of potassium by muscle and the liver. Moreover, β-adrenergic blockade can impair the handling of a potassium load in some patients.
Acute increases in plasma osmolality (hyper-natremia, hyperglycemia, or mannitol administra-tion) may increase plasma [K+] (about 0.6 mEq/L per 10 mOsm/L). In such instances, the movement of water out of cells (down its osmotic gradient) is accompanied by movement of K+ out of cells. The latter may be the result of “solvent drag” or the increase in intracellular [K+] that follows cellular dehydration.
Hypothermia has been reported to lower plasma [K+] as a result of cellular uptake. Rewarm-ing reverses this shift and may result in transient hyperkalemia if potassium was given during the hypothermia.
Urinary potassium excretion generally parallels its extracellular concentration. Potassium is secreted by tubular cells in the distal nephron. Extracellular [K+] is a major determinant of aldosterone secre-tion from the adrenal gland. Hyperkalemia stimu-lates aldosterone secretion, whereas hypokalemia suppresses aldosterone secretion. Renal tubular flow in the distal nephron may also be an impor-tant determinant of urinary potassium excretion because high tubular flow rates (as during osmotic diuresis) increase potassium secretion by keeping the capillary to renal tubular gradient for potassium secretion high. Conversely, slow tubular flow rates increase [K+] in tubular fluid and decrease the gradi-ent for K+ secretion, thereby decreasing renal potas-sium excretion.