Intracellularly regulated Ca2+ influx or remnants of extracellularly activated signalling pathway in human
Department of Biochemistry and Microbiology, Faculty of Chemical and Food Technology, Slovak University of Technology, 812 37- Bratislava, Slovak Republic
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Abstract: Phorbol-14-myristate-13-acetate (PMA) (10-7-10-6 mol/l) inhibited the Ca2+-dependent K+ efflux (the Gárdos effect - GE) induced by Ca2+, the hyperpolarisation accompanying the GE, the vanadate-induced 45Ca2+ influx, and depolarised the membrane, in vanadate-treated human red blood cells (RBC). The GE induced by propranolol (PLL) was not inhibited by PMA. Both PMA and PLL stimulated the basal 45Ca2+ influx. These results suggest that a) protein kinase C activity prevents the activation of GE by vanadate but PLL bypasses this mechanism, b) the stimulation of the Ca2+ influx by PMA and the GE inhibition are caused by the membrane depolarisation, c) the basal Ca2+ influx in human RBC is regulated in a complex manner, and d) the effect of vanadate resembles to the activation of agonist-stimulated signalling pathway in non-excitable cells.
Keywords: Human red blood cells; Ca2+ influx; Gárdos effect; Ca2+-activated K+ channel, propranolol; vanadate; PMA
Full paper in Portable Document Format: acs_0017.pdf
Acta Chimica Slovaca, Vol. 1, No. 1, 2008, pp. 180—191