Recombinant human erythropoietin has no direct or strong vasoconstrictor effects in vivo and in vitro.

An elevation of blood pressure is observed in approximately 30% of dialysis patients treated with recombinant human erythropoietin (rHuEPO). Various studies have been performed in order to elucidate possible underlying mechanisms, but it is not yet well understood whether there is one major mechanism involved. In this present study, samples were obtained from male normotensive Wistar-Kyoto rats (WKY) and genetically hypertensive rats (SHR) at the age of 5 and 20 weeks. Thoracic aorta rings, with or without endothelium, isolated from WKY and SHR were used to evaluate the direct effect of rHuEPO on vascular smooth muscle by measuring the tension of vascular smooth muscle induced by various concentrations (1-100 IU/ml) of rHuEPO. Also, rHuEPO (10, 100, 1000 and 10,000 IU/kg) was intravenously administrated and the changes in mean blood pressure were recorded for 5-10 min. rHuEPO produced no significant contraction in the rat aortae in any of the preparation studies, in the presence or the absence of endothelium. The intravenous administration of rHuEPO had no immediate effect on mean blood pressure in 5- and 20-week-old WKY and SHR. These results suggest that the elevation of blood pressure observed in the clinical setting following the administration of rHuEPO is not due to a direct pressor effect on vascular smooth muscle.