The pressor effect of recombinant human erythropoietin is not due to decreased activity of the endogenous nitric oxide system

D. Del Castillo, L. Raij, P. J. Shultz, J. P. Tolins

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

In a subset of dialysis patients, erythropoietin (rHuEpo) treatment exacerbates hypertension. The mechanism of this presser effect is unknown; however, it has been suggested that decreased endogenous nitric oxide (NO) activity may play a role. To explore this hypothesis, Sprague-Dawley rats were given rHuEpo (150 U/kg s.c. three times per week) or corresponding vehicle. Blood pressure, haematocrit, and urinary excretion of the stable NO metabolites, nitrite (NO2) and nitrate (NO3), were determined at baseline and 3 weeks. After 3 weeks of rHuEpo treatment there was a significant increase in blood pressure and haematocrit, while in vehicle-treated rats blood pressure and haematocrit remained at basal levels. Urinary excretion of NO2 + NO3 increased compared to basal in rHuEpo, but not vehicle rats. Thus in normal rats rHuEpo does have a significant presser effect, but this is not associated with decreased activity of the endogenous NO system. Thus decreased endogenous NO activity is not responsible for rHuEpo-associated hypertension. These data further suggest that endogenous NO activity is increased in rHuEpo-treated rats, perhaps as a counter-regulatory mechanism that limits the presser effect. Whether this mechanism is active in the setting of rHuEpo-treated chronic renal failure in humans is unknown.

Original languageEnglish (US)
Pages (from-to)505-508
Number of pages4
JournalNephrology Dialysis Transplantation
Volume10
Issue number4
DOIs
StatePublished - Apr 1995

Keywords

  • Erythropoietin
  • Hypertension
  • Nitric oxide
  • NO

ASJC Scopus subject areas

  • Nephrology
  • Transplantation

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