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The Effects of Pentoxifylline on the Plasma Membrane Ca 2+ ATPase in Age‐Separated Rat and Human Erythrocytes
Author(s) -
Seidler Norbert W.,
Swislocki Norbert I.
Publication year - 1992
Publication title -
the journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.92
H-Index - 116
eISSN - 1552-4604
pISSN - 0091-2700
DOI - 10.1002/j.1552-4604.1992.tb03844.x
Subject(s) - pentoxifylline , membrane , atpase , human plasma , chemistry , pharmacology , endocrinology , medicine , biophysics , biochemistry , enzyme , chromatography , biology
Pentoxifylline, a dimethyl xanthine derivative given to patients with peripheral vascular disorders, increases erythrocyte deformability, diminishes Ca 2+ entry, inhibits Ca 2+ ‐dependent transglutaminase activity and elevates ATP levels. The present study examined the effects of pentoxifylline on the Ca 2+ pump ATPase, an enzyme which regulates intracellular Ca 2+ levels. Studies were carried out with inside‐out vesicles (IOVs) prepared from young (Ey) and old (Eo) human and rat erythrocytes. The pumping of Ca 2+ depends on the concomitant hydrolysis of ATP; the two processes were measured using radiolabeled substrates. The catalytic properties of IOVs from young and old erythrocytes were stimulated by pentoxifylline when added directly to the assay medium. Pentoxifylline (0.5 to 5.0 mM) significantly activated the rates of Ca 2+ dependent ATP hydrolysis in Ey and Eo IOVs of rat erythrocytes. The percent of activation was greater in the IOVs from older erythrocytes. The Ca 2+ translocation was also affected by pentoxifylline. The early burst of Ca 2+ uptake into IOVs decreased in the presence of pentoxifylline in Ey IOVs prepared from either species whereas steady state rates of Ca 2+ transport only declined at 5.0 mM pentoxifylline. This pattern was not evident in the corresponding Eo IOVs. The response of Ey and Eo IOVs to pentoxifylline may be the basis of the difference in sensitivity of young and old erythrocytes to the drug in regulating intracellular Ca 2+ concentrations.