Artikel
Impaired stimulated NO-activity by Erythropoietin in Hypertensive but not in Normotensive
Gestörte Stimulierbarkeit der NO-Aktivität bei Hypertonikern nach Erythropoietingabe gegenüber Normotonikern
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Veröffentlicht: | 11. November 2004 |
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Gliederung
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Background
Arterial hypertension is the major side effect of erythropoietin (Epo). We examined nitric oxide activity of the forearm artery after Epo in normotensive and hypertensive patients.
Methods
In a randomized, double blind, placebo-controlled cross-over study Epo (66U/kg body weight AranespR) or placebo was administered i.v. to 17 normotensive subjects and 17 patients with mild essential hypertension. All participants were young males, non-smokers, had no diabetes, hypercholesteremia or antihypertensive medication. After 24 hours we evaluated the response of forearm blood flow (FBF) to i.a. given acetycholine, an endothelium-dependent vasodilator, to nitroprussid, an endothelium-independent vasodilator, and to N-monomethyl-L-arginine (L-NMMA), an inhibitor of endothelial NO synthase. FBF was measured at baseline and during pharmacologic tests by strain-gauge plethysmography.
Results
After a single injection of Epo no changes of blood pressure were observed in normotensive and hypertensive patients by 24 hour ambulatory blood pressure monitoring. The FBF in response to acetylcholine (12 µg/min) increased after Epo in the normotensive group (Delta FBF 6.70±6.12 mL/min vs. placebo 4.09±2.82 mL/min p=0.05), but not in the hypertensive group (Delta FBF 4.4±3.07 vs. placebo 4.94±4.10 mL/min n.s.). In response to nitroprussid (12.8µg/min) the FBF increased more marked after Epo in normotensive subjects (Delta FBF 17.88±5.87 vs. placebo 12.48± 4.44 mL/min p=0.012), but not in hypertensive patients (Delta FBF 16.33±5.26 vs. placebo 14.33±5.27 mL/min n.s.). There were no differences in FBF changes due to L-NMMA for both groups.
Conclusion
A single injection of Epo leads to an enhanced response to endothelium-dependent and -independent vasodilators in normotensive but not in hypertensive subjects. These findings suggest that Epo leads to compensatory increased vasodilation in normotensive subjects, but no such counter-reaction was found in hypertensive patients.