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 language | English (US) |
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Pages (from-to) | 505-508 |
Number of pages | 4 |
Journal | Nephrology Dialysis Transplantation |
Volume | 10 |
Issue number | 4 |
DOIs | |
State | Published - Apr 1995 |
Keywords
- Erythropoietin
- Hypertension
- Nitric oxide
- NO
ASJC Scopus subject areas
- Nephrology
- Transplantation