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New vanadate‐induced Ca 2+ pathway in human red cells
Author(s) -
Romero Pedro J.,
Romero Eneida A.
Publication year - 2003
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2003.07.002
Subject(s) - vanadate , biophysics , chemistry , stimulation , calcium , mechanism of action , metabolism , ion transporter , biochemistry , biology , endocrinology , membrane , in vitro , organic chemistry
Vanadate is a commonly used Ca 2+ pump blocker, exerting a substantial effect on Ca 2+ extrusion at millimolar concentrations in human red cells. At such levels, vanadate also seems to open an L type‐like Ca 2+ channel in these cells (J Biol Chem 257 (1982) 7414; Gen Physiol Biophys 16 (1997) 359). Since neither a dose‐dependence effect nor a metabolic requirement for the latter action could be found in the literature, we have addressed this matter in the present work. Accordingly, vanadate action on Ca 2+ entry was systematically investigated in both young and old human red cells after metabolic depletion. Although vanadate enhanced Ca 2+ entry indifferently in either cell type, a distinct over‐all effect was paradoxically found depending on whether or not metabolic substrates that give rise to ATP were present. In ATP‐depleted cells, unlike with ATP‐containing cells, vanadate‐stimulated Ca 2+ entry was neither blocked by raising external K + nor by adding voltage‐dependent Ca 2+ channel blockers (nifedipine, calciseptine, FTX3.3) or compounds affecting polyphosphoinositide metabolism (Li + , neomycin). Likewise, full substitution of external Na + by other cations did not inhibit vanadate‐enhanced Ca 2+ entry. Regardless of the cell age, stimulation by vanadate depended strongly on internal Na + (0–30 mM). Vanadate stimulation was significantly reduced (about 55%) by heparin (10 mg/ml) only in young cells and by ryanodine (about 35%, 250 μM) in old cells. The results suggest presence of a new vanadate‐induced Ca 2+ entry pathway in ATP‐depleted cells.