Na+-K+ transport and volume of rat erythrocytes under dietary K+ deficiency

Abstract

Red cell Na+ and K+ content and transport were studied in Sprague-Dawley rats in the course of a dietary K+ depletion ranging 1-6 wk. Plasma K+ fell to below 2 mM, and red cell K+ decreased. Cellular Na+ rose due to an increase of the Na+ leak. Inward Rb+ and outward Na+ transport by the Na+-K+ pump (determined at 2 mM external Rb+) were accelerated by the rise in cell Na+ concentration. K+ depletion caused a cation deficit of up to 30% of total red cell Na+ plus K+ and a consecutive cell shrinkage with an increase in mean cellular hemoglobin content (MCHC). The cell shrinkage, in turn, was paralleled by up to a 10-fold increase in the maximum capacity of the furosemide-sensitive, chloride-dependent Na+-K+ cotransport system. This system participated with up to 50% of the total K+ movements across the red cell membrane in severe K+ deficiency. In normal cells shrunken by osmotic means, Na+-K+ cotransport was similarly accelerated severalfold, indicating that the cell shrinkage occurring during K+ depletion is a major factor inducing the changes in Na+-K+ cotransport. However, a second unknown factor is also involved. It is concluded that in the rat, not only genetic but also environmental parameters contribute in determining the actual activity of the red cell Na+-K+ cotransport system. The cell volume and MCHC must be considered when judging Na+ and K+ transport changes observed in rat erythrocytes under various pathophysiological conditions.

Role of the furosemide-sensitive Na+/K+ transport system in determining the steady-state Na+ and K+ content and volume of human erythrocytesin vitro andin vivo

“…It thus differs from the regulatory volume decrease and the response towards catecholamines found in bird erythrocytes [29,32,34] and from the "uncoupling" of Na + from K + movements seen in swollen human erythrocytes [1]. Finally, furosemide-sensitive K + transport is not [11] or only slightly [1] volume dependent in human erythrocytes, in contrast to the system found in bird [25,29,32,40] and rat erythrocytes [12,13].…”

“…9 are the calculated working points of the furosemide-sensitive transport system in erythrocytes of normal (A) and K+-depleted rats (B) [12]. The furosemidesensitive transport system of rat erythrocytes is similar to that of human erythrocytes, except that the maximum transport rates in the rat increase more than 10-fold upon cell shrinkage [12,13], a phenomenon not seen with human erythrocytes [11]. Due to the low stationary Na + concentration in normal rat erythrocytes the furosemide-sensitive transport system should work in the inward direction.…”

“…Due to the low stationary Na + concentration in normal rat erythrocytes the furosemide-sensitive transport system should work in the inward direction. The fall in plasma K + and the increase in red cell Na + in rats depleted of K § due to dietary K + restriction [12] should favor outward net transport, indicating that the net effect of the bidirec-tionally operating transport system may drastically change under severe electrolyte disturbances. With respect to furosemide-sensitive Na + movements, the above predictions were found to be fulfilled in rat erythrocytes [12].…”

Volume-dependent regulation of ion transport and membrane phosphorylation in human and rat erythrocytes

“…The osmotic swelling of human erythrocytes increased the furosemide-inhibited component of 86Rb influx only by 30-40% (O'Neill & Mikkelsen, 1987). A negligible increase (10-20%) of the rate of 86Rb influx was observed in osmotically shrunken rat erythrocytes (Duhm & G6bel, 1984b). Adragna and Tosteson (1984) demonstrated a reduction in furosemide-sensitive potassium efflux with isosmotic, but not osmotic, cell swelling and an increase in furosemide-sensitive sodium ef-flux with isosmotic shrinkage of human erythrocytes treated with 2,5-chloromercuribenzoate.…”

Membrane Mechanisms in Volume Regulation in Vertebrate Cells and Epithelia

“…A role for Na + ,Cl-or Na +,K + ,2CI-cotransport in cell volume regulation has, in addition to avian red blood cells, Ehrlich cells, and frog skin epithelial cells (see above), also been established in red blood cells from rat [56] and ferret [226] and in L cells [86], simian virus-transformed 3T3 cells [15], chick cardiac cells [80], astrocytes from rat cerebral cortex [156], and the apical membrane of rabbit kidney medullary thick ascending limb of Henle's loop (see review by Eve10ff and Warnock [70]). (It may be noted that the Na +,K + ,2CI-cotransport system in red blood cells from other species, e.g., humans [57], is volume insensitive.)…”