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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 (pH_i). 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 Ca_i²⁺ (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 Ca_i²⁺ 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 alpha^2A-adrenergic receptors on protein kinase C.