Miriam Zacchia1, Maria Luisa Abategiovanni1, Spiros Stratigis2, Giovambattista Capasso1. 1. Section of Nephrology, Department of Cardiothoracic and Respiratory Sciences, Second University of Naples, Naples, Italy, Heraklion, Greece. 2. Department of Nephrology, University Hospital of Heraklion, Heraklion, Greece.
Abstract
BACKGROUND: Potassium (K(+)) is the major intracellular cation, with 98% of the total pool being located in the cells at a concentration of 140-150 mmol/l, and only 2% in the extracellular fluid, where it ranges between 3.5 and 5 mmol/l. A fine regulation of the intracellular-extracellular gradient is crucial for life, as it is the main determinant of membrane voltage; in fact, acute changes of K(+) plasma levels may have fatal consequences. SUMMARY: An integrated system including an 'internal' and 'external' control prevents significant fluctuations of plasma levels in conditions of K(+) loading and depletion. The internal control regulates the intra-extracellular shift, a temporary mechanism able to maintain a constant K(+) plasma concentration without changing the total amount of body K(+). The external control is responsible for the excretion of the ingested K(+), and it has the kidney as the major player. The kidney excretes nearly 90% of the daily intake. Along the proximal tubule and the thick ascending limb on Henle's loop, the amount of K(+) reabsorption is quite fixed (about 80-90%); conversely, the distal nephron has the ability to adjust K(+) excretion in accordance with homeostatic needs. The present review analyzes: (1) the main molecular mechanisms mediating K(+) reabsorption and secretion along the nephron; (2) the pathophysiology of the principal K(+) derangements due to renal dysfunction, and (3) the effect of ingested K(+) on blood pressure and renal electrolyte handling. KEY MESSAGES: Maintaining plasma K(+) levels in a tight range is crucial for life; thus, multiple factors are implicated in K(+) homeostasis, including kidney function. Recent studies have suggested that K(+) plasma levels, in turn, affect renal salt absorption in animal models; this effect may underlie the reduction of blood pressure observed in hypertensive subjects under K(+) supplementation.
BACKGROUND:Potassium (K(+)) is the major intracellular cation, with 98% of the total pool being located in the cells at a concentration of 140-150 mmol/l, and only 2% in the extracellular fluid, where it ranges between 3.5 and 5 mmol/l. A fine regulation of the intracellular-extracellular gradient is crucial for life, as it is the main determinant of membrane voltage; in fact, acute changes of K(+) plasma levels may have fatal consequences. SUMMARY: An integrated system including an 'internal' and 'external' control prevents significant fluctuations of plasma levels in conditions of K(+) loading and depletion. The internal control regulates the intra-extracellular shift, a temporary mechanism able to maintain a constant K(+) plasma concentration without changing the total amount of body K(+). The external control is responsible for the excretion of the ingested K(+), and it has the kidney as the major player. The kidney excretes nearly 90% of the daily intake. Along the proximal tubule and the thick ascending limb on Henle's loop, the amount of K(+) reabsorption is quite fixed (about 80-90%); conversely, the distal nephron has the ability to adjust K(+) excretion in accordance with homeostatic needs. The present review analyzes: (1) the main molecular mechanisms mediating K(+) reabsorption and secretion along the nephron; (2) the pathophysiology of the principal K(+) derangements due to renal dysfunction, and (3) the effect of ingested K(+) on blood pressure and renal electrolyte handling. KEY MESSAGES: Maintaining plasma K(+) levels in a tight range is crucial for life; thus, multiple factors are implicated in K(+) homeostasis, including kidney function. Recent studies have suggested that K(+) plasma levels, in turn, affect renal salt absorption in animal models; this effect may underlie the reduction of blood pressure observed in hypertensive subjects under K(+) supplementation.