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- W2102600144 abstract "Elevation of the cytoplasmic Ca2+ concentration ([Ca2 +]i) by epinephrine and epinephrine-induced inhibition of prostaglandin E1 (PGE1)-stimulated cyclic adenosine monophosphate (CAMP) accumulation were assessed in platelets from three groups of subjects: normal controls (NS, n = 11) and patients with myeloproliferative disorders whose platelets were either sensitive (ES, n = 9) or specifically insensitive (El, n = 7) to the aggregatory effect of epinephrine. The inhibition by epinephrine of CAMP accumulation in the platelets exposed to 500 nM PGE, was not significantly different between the three groups. Therefore, despite the detective aggregation response to epinephrine, platelets from the El group seemed to retain normal response, which was attained through cα2-adrenergic receptors, guanine nucleotide binding regulatory protein, and the adenylate cyclase system. However, in aequorin-loaded, washed platelets, the epinephrine-stimu-lated rise in [Ca2+]i showed significant decrease in the El group compared with the other groups (P < 0.01). Thus the mechanism for the impaired aggregation response to epinephrine in platelets from the El group could include the defect that exists in the pathway from receptor binding of epinephrine to the aggregation response through [Ca2+]i elevation." @default.
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- W2102600144 title "Deficient elevation of the cytoplasmic calcium ion concentration by epinephrine in epinephrine-insensitive platelets of patients with myeloproliferative disorders" @default.
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- W2102600144 doi "https://doi.org/10.1002/ajh.2830330205" @default.
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