Prostaglandin E, (PGE,) increases the deformability of red blood cells by decreasing cell volume, while PGE2 has the opposite effect. This takes place within seconds and requires low, physiological doses of prostaglandin. They may be important in controlling capillary circulation. These effects may play a role in the evolution of shock and essential hypertension. PGE has induced sickling in susceptible cells. PGE, inhibits while PGE2 potentiates platelet aggregation induced by a variety of agents. These effects seem to be modulated by cyclic adenosine monophosphate levels, which are increased by PGE, and decreased by PGE2. Antiaggregation properties of PGE, markedly increase the poststorage yield of functional platelets for transfusion. Erythropoiesis is stimulated both by a direct effect on erythroid precursor cells and by stimulating erythropoietin release from kidneys of animals infused with PGE1.