![]() ![]() Conversely, net cellular uptake of K + is observed in metabolic alkalosis with alkalemia. 1, 4 In general, metabolic acidosis with acidemia causes a net shift of K + from the intracellular to the extracellular space. 12 – 17 Interaction of K +-Cl − cotransport with acid-base transport will be discussed later.Īcute effects of acid-base disturbances on K + redistribution have long been known. Expression of K +-Cl − cotransporters KCC1, KCC3, and KCC4, as well as Na +-K +-Cl − cotransporter NKCC1, has been detected in skeletal muscle. Cation-chloride cotransport pathways are also present. 11 During conditions like lactic acidosis, this pathway will mediate influx of H + and lactate, resulting in decreased intracellular pH. Monocarboxylate cotransporters, MCT1 and MCT4, are expressed in skeletal muscle. Another pathway of potential importance for cellular acid-base homeostasis is monocarboxylate cotransport that mediates coupled flux of H + with such organic anions as lactate ( Figure 2). ![]() In addition, isoforms of the Na +-bicarbonate cotransporter, NBCe1 and NBCe2, are expressed in muscle, raising the possibility that Na +-HCO 3 − cotransport contributes to intracellular pH regulation, 10 as also indicated in Figure 2. 9Ī lesser component of intracellular pH regulation in skeletal muscle is HCO 3-dependent, because of Cl −-HCO 3 − exchange, 7 also shown in Figure 2. 7 Na +-H + exchanger isoform NHE1 is expressed in skeletal muscle and presumably accounts for most Na +-H + exchange activity in this tissue. 8 Activity of this pathway in response to acid-base perturbations strongly affects intracellular Na + loading. Na +-H + exchange in skeletal muscle is highly dependent on intracellular pH, with marked activation by intracellular acidity and inhibition by alkalinity. 6 Quantitatively, the most important pathway regulating intracellular pH in skeletal muscle is Na +-H + exchange, 7 as shown in Figure 2. However, muscle cells have additional pathways regulating intracellular pH homeostasis that can indirectly affect cellular Na + and K + balance. 5 Accordingly, cell ion content is determined by the balance between pump and leak pathways for Na + and K +. The electrochemical gradients of Na + and K + are restored by active Na + extrusion and K + uptake by the Na +,K +-ATPase. Cl − channels play an important role in stabilizing the membrane potential and contributing to repolarization after action potentials. Muscle contraction is triggered by action potentials involving depolarizing Na + entry through Na + channels followed by membrane repolarization mediated by K + efflux through K + channels. Multiple ion transport pathways directly or indirectly affect net K + flux in skeletal muscle cells. ![]() Thus, plasma K + is at the mercy of the interplay between internal K + distribution and external K + balance mediated by renal K + excretion. Second, as also illustrated in Figure 1, in steady state the typical daily K + ingestion of about 70 mEq/d would be sufficient to cause large changes in extracellular K + were it not for continuous renal K + excretion, because K + loss from the gastrointestinal tract is quite modest under normal conditions. 3, 4 Rapid redistribution of K + into the intracellular space is essential for minimizing increases in extracellular K + concentration during acute K + loads. As described in Figure 1, many factors in addition to acid-base perturbations modulate internal K + distribution including insulin, catecholamines, and hypertonicity. First, as illustrated in Figure 1, because some 98% of the total body content of K + resides within cells, predominantly skeletal muscle, small acute shifts of intracellular K + into or out of the extracellular space can cause severe, even lethal, derangements of extracellular K + concentration. 2 However, maintenance of normal extracellular K + (3.5 to 5 mEq/L) is under two potential threats. 1 Maintenance of extracellular K + concentration within a narrow range is vital for numerous cell functions, particularly electrical excitability of heart and muscle. The effects of acid-base balance on serum potassium are well known. ![]()
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