Intracellularly regulated Ca influx or remnants of extracellularly activated signalling pathway in human red blood cells?

Phorbol-14-myristate-13-acetate (PMA) (10-10 mol/l) inhibited the Ca-dependent K efflux (the Gárdos effect GE) induced by Ca, the hyperpolarisation accompanying the GE, the vanadate-induced Ca 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 Ca 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 Ca influx by PMA and the GE inhibition are caused by the membrane depolarisation, c) the basal Ca influx in human RBC is regulated in a complex manner, and d) the effect of vanadate resembles to the activation of agoniststimulated signalling pathway in non-excitable cells.