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Research Article Free access | 10.1172/JCI114039
Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, Massachusetts 02115.
Find articles by Halperin, J. in: JCI | PubMed | Google Scholar
Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, Massachusetts 02115.
Find articles by Brugnara, C. in: JCI | PubMed | Google Scholar
Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, Massachusetts 02115.
Find articles by Nicholson-Weller, A. in: JCI | PubMed | Google Scholar
Published May 1, 1989 - More info
The lytic effect of complement on human erythrocytes has been reported by others to increase when Na+ is substituted for K+ in the external medium. In this paper we have investigated the hypothesis that net loss of K+ through a K+ transport pathway protects erythrocytes from complement-induced colloidosmotic swelling and lysis. Antibody-sensitized human erythrocytes containing different intracellular cation concentrations (nystatin treatment) were exposed to low concentrations of guinea pig serum in media of different cation composition; complement lysis was assessed by the release of hemoglobin and the volume of the surviving cells estimated by their density distribution profiles. Complement-dependent swelling and lysis of erythrocytes (a) were limited by the presence of an outwardly directed K+ electrochemical gradient and (b) were enhanced by carbocyanine, a specific inhibitor of the Ca2+-activated K+ transport pathway, and by absence of Ca2+ in the external medium. We propose that during complement activation a rising cytosolic calcium triggers the Ca2+-activated K+ permeability pathway, the Gardos effect, produces a net K+, Cl- and water loss, and thus limits the colloidosmotic swelling and lysis of erythrocytes.