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Free keywords:
Epinephrine; Sodium ion-proton exchange; Intracellular pH; pH, intracellular;
(Platelet)
Abstract:
In the present study, we investigated whether stimulation of platelets by epinephrine affects the Na+/H+ exchanger, an antiport that regulates the cytosolic pH (pHi). Epinephrine alone failed to modulate Na+/H+ exchange, as reflected by a constant fluorescence of the pHi indicator BCECF. In contrast, epinephrine accelerated Na+/H+ exchange upon stimulation with a threshold concentration of platelet activating factor (PAF). The extra Na+/H+ exchange was not caused by a better binding of PAF to platelets and occurred also in the presence of indomethacin, excluding a role for cyclooxygenase products. Epinephrine failed to mobilize Cai2+ (measured by fura-2 fluorescence) and did not activate protein kinase C ([32P]pleckstrin) or phospholipase C ([32P]phosphatidic acid). In combination with PAF, epinephrine left the PAF-induced mobilization of Cai2+ and accumulation of [32P]phosphatidic acid unchanged, but induced a 1.3-fold increase in the phosphorylation of pleckstrin. These data indicate that epinephrine enhances Na+/H+ exchange via a direct effect of alpha2A-adrenergic receptors on protein kinase C.
