Ion transport, membrane potential, and cytoplasmic pH in lymphocytes: changes during activation

Calcium-activated potassium channels in resting and activated human T lymphocytes. Expression levels, calcium dependence, ion selectivity, and pharmacology.

“…Preliminary fluorescent-indicator studies on individual cells indicate that oscillations in membrane potential accompany the [Ca2+]i oscillations in Jurkat T cells (Lewis, Grissmer, and Cahalan, 1991). The hyperpolarization can be explained by the presence of K + channels that are activated by [Ca2+]i, a conclusion supported by measurements of S6Rb+ efflux from cells stimulated with Ca2+-mobilizing agents (reviewed by Rink and Deutsch, 1983;Grinstein and Dixon, 1989). These K + channels, by hyperpolarizing the membrane, may facilitate mitogen-regulated Ca 2+ entry, since a combination of voltage-and calcium-activated K + channel blockers has been shown to inhibit mitogen-induced Ca 2+ oscillations in Jurkat T cells (Grissmer, Lewis, and Cahalan, 1992b).…”

“…Although Ca 2+ entry across the plasma membrane would be expected to depolarize the cell, several studies of human T and B cells and mouse thymocytes have shown instead that membrane hyperpolarization accompanies the rise in [Ca2+]i (Tsien et al, 1982;Felber and Brand, 1983;Wilson and Chused, 1985;Tatham, O'Flynn, and Linch, 1986;MacDougall, Grinstein, and Gelfand, 1988; reviewed by Grinstein and Dixon, 1989). Preliminary fluorescent-indicator studies on individual cells indicate that oscillations in membrane potential accompany the [Ca2+]i oscillations in Jurkat T cells (Lewis, Grissmer, and Cahalan, 1991).…”

Long‐term enhancement of Na,K‐ATPase pump during blasttransformation of human lymphocytes is controlled first by translational, then by transcriptional mechanisms

“…Potassium influx via the Na,K-ATPase pump has been shown to increase significantly in animal cells stimulated from quiescence to proliferation: a rapid elevation of the ion pump flux in response to mitogens is followed by a long-term increase in the pump activity in the course of the G0/GI/S transition [1][2][3][4][5]. The initial activation of the Na,K-ATPase pump has been considered to result from the elevation of intracellular Na concentration (Na3 due to an enhanced Na/H exchange [2,6].…”

Regulation of intracellular pH in the spontaneously hypertensive rat. Role of bicarbonate-dependent transporters.

“…25 - 29 Both transporters thus regulate pH, and sodium entry into the cell. 22 Overactrvity of either one or both of these transporters, particularly if accompanied by reduced sodium extrusion via the plasma membrane Na + ,K + -ATPase pump, would explain the elevated levels of intracellular sodium recently reported by us in lymphocytes from the spontaneously hypertensive rat (SHR) 34 and by others in red blood cells of subjects with primary hypertension. 35 In the present study we examined the activity of the Na + -H + antiporter in the presence of HCO 3 -CO 2 as well as the activity and kinetic properties of the Na + -dependent and Na + -independent C1"-HCO 3 " exchangers using freshly isolated lymphocytes from SHR and WistarKyoto (WKY) rats.…”

“…This, by design, results in an overestimation of the role of the Na + -H + antiporter in the regulation of intracellular pH (pH|) and ignores the existence of other HCO 3~-dependent transporters that contribute not only to the regulation of pH| 15 -17 but also to the regulation of cell volume, 1819 cell growth, 2021 and intracellular sodium. 22 Alterations in the control of any or all of these processes could in various ways be involved in the pathogenesis of hypertension. 2 -3910 - 23 Exploration of the activity and kinetic properties of the various pH, regulatory transporters therefore seems a logical step in the evaluation of pH r regulating mechanisms in cells from hypertensive subjects.…”