Abstract
This study aimed at establishing the role of calmodulin in regulating pH i of human platelets under acid loads and in stimulated states. The response of human platelets to thrombin was an initial drop of pH i followed by a recovery with a significant increase above the pre-stimulation level in control experiments and a recovery to initial values in platelets maintained in the presence of 19 mmol/l TFP (trifluoperazine = 2 trifluoromethyl-10 [3'-(1 methyl-4-piperazinyl) propyl] pheno-thiazine). The change in pH i after 8 min was 0.130 ± 0.030 in the control and 0.001 ± 0.011 pH units in TFP (P <0.05). The initial velocity of recovery from an acid load was reduced to 56.7 ± 6% of the control (n = 6, P < 0.05) with 50 µmol/l W7 (N-(6 aminohexyl)-5-chloro-1-naphthalene sulphonamide), and to 29.7 ± 4.3% of the control (n = 8, P < 0.05) with 19 µmol/l TFP. The initial velocity of recovery was significantly greater in recalcified platelets than in the preparations kept in the nominal absence of extracellular calcium (1.08 ± 0.12 vs 0.66 ± 0.12 pH units per min, P < 0.05). Lower concentration of TFP had an inhibitory effect only in the presence of calcium. The velocities of recovery reached similar values at higher TFP concentration. The significant interaction between Ca 2+ and TFP concentrations indicates that the Ca-calmodulin complex, rather than an unspecified direct action of TFP, is responsible for the modulation of the Na + /H + exchanger. These findings indicate that calcium-calmodulin participates in both the recovery of pH after an acid load and the increase of pH i in stimulated states of human platelets.
Published Version
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