Abstract
In viable human erythrocytes, passive downhill entry of Ca2+ through the plasma membrane is opposed by an active extrusion Ca2+-pump mechanism which maintains a free [Ca2+]i approximately 10(-7) M. This passive Ca2+ permeability can be determined reliably in cells with a completely arrested Ca2+ pump, as can be achieved in cells which are both ATP-depleted and vanadate-treated. With this approach, whole-cell preparations from banked human erythrocytes exhibited passive net uptake of Ca2+ that has characteristics of a carrier-mediated process which could be shunted by the addition of the Ca2+ ionophore A23187. Passive Ca2+ uptake was apparently independent of extracellular Na+, K+ or Cl- and was not responsive to a variety of Ca2+ channel entry blockers. However, in the presence of phenylglyoxal, a specific, covalent modifier of arginyl residues, the initial (0 to 60 min) rate of passive Ca2+ uptake was inhibited in a dose-dependent manner. This can be taken in support of a proteinaceous carrier-mediated passive Ca2+ entry mechanism that involves one or several functional arginyl residue(s) and may represent Ca2+ back-diffusion through the arrested Ca2+ translocation pump.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
