Magnitude of calcium influx required to induce dehydration of normal human red cells

Teresa Tiffert, Jerry L Spivak, V. L. Lew

Research output: Contribution to journalArticle

Abstract

Activation by [Ca2+]i of Ca2+-sensitive K+ channels has long been known to cause dehydration of red cells suspended in low-K, plasma-like media. However, the fundamental question of the extent to which Ca influx must be increased to trigger dense cell formation in conditions likely to arise in the circulation has not been established. We report here that in ionophore permeabilized red cells, increasing Ca influx above 0.7 mmol/litre cells per h induces the formation of subpopulations of dehydrated cells within 1-2 hours. The presence or absence of glycolytic substrates had little effect suggesting that ATP depletion was not large enough to significantly inhibit the pump within that period. Below maximal dehydrating Ca influxes of about 1.2 mmol/litre cells per h, the trend was for the fraction of dense cells formed to remain steady in time. As Ca influx was increased, both the rate of dense cell formation and the fraction of dense cells formed increased. These results are analyzed in relation to mechanisms and to possible states of increased Ca2+ permeability in physiological and physiopathological conditions.

Original languageEnglish (US)
Pages (from-to)157-165
Number of pages9
JournalBBA - Biomembranes
Volume943
Issue number2
DOIs
StatePublished - Aug 18 1988

Fingerprint

Dehydration
Cells
Calcium
Ionophores
Adenosine Triphosphate
Chemical activation
Pumps
Plasmas
Substrates
Permeability

Keywords

  • (Human)
  • Calcium dependence
  • Calcium flux
  • Calcium ion
  • Erythrocyte
  • intracellular
  • Potassium channel
  • Volume regulation

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology

Cite this

Magnitude of calcium influx required to induce dehydration of normal human red cells. / Tiffert, Teresa; Spivak, Jerry L; Lew, V. L.

In: BBA - Biomembranes, Vol. 943, No. 2, 18.08.1988, p. 157-165.

Research output: Contribution to journalArticle

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