Prostaglandin E2 effects on cation flux in sickle erythrocyte ghosts.
Prostaglandin E2 has previously been shown to enhance the shape transformation of sickle prone erythrocytes (8) and to reduce the oxygen resaturation of Hemoglobin SS within intact sickle cell erythrocytes after deoxygenation (15). In view of the recent importance attributed to calcium transport in maintaining erythrocyte shape and viability (10) and the suggestion that prostaglandins may act via a calcium ionophore mechanism (9) on cell membranes, erythrocyte ghosts were prepared following the method of Lepke and Passow (12) from normal and sickle cell anemia erythrocytes. These two classes of ghosts are shown to display differing patterns of sodium and calcium transport, whith calcium influx being preferentially stimulated by prostaglandin E2 in sickle cell ghosts. It is suggested that in hypoxic, stasis conditions in vivo, prostaglandins may play a role in accelerating sickling of sickle prone erythrocytes via stimulation of calcium influx.
D000755:Anemia, Sickle Cell / Q000097:blood*; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000097:blood*; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D003864:Depression, Chemical; D004912:Erythrocytes / Q000378:metabolism; D004913:Erythrocytes, Abnormal / Q000378:metabolism*; D006451:Hemoglobin, Sickle / Q000378:metabolism; D006801:Humans; D010042:Ouabain / Q000494:pharmacology; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D011458:Prostaglandins E / Q000494:pharmacology*; D012964:Sodium / Q000097:blood*; D013268:Stimulation, Chemical; D013997:Time Factors
D006451:Hemoglobin, Sickle; D011458:Prostaglandins E; D010042:Ouabain; D012964:Sodium; D010100:Oxygen; D002118:Calcium