Hand MF, Haynes WG, Johnstone HA, Anderson JL, Webb DJ
Erythropoietin enhances vascular responsiveness to
norepinephrine in renal failure
Kidney Int
(Sep) 48:806-813 1995
Increased blood pressure into the hypertensive range or
worsening hypertension after erythropoietin (EPO) therapy in
hemodialysis patients is a well recognized clinical phenomenon; however,
the mechanism of EPO-induced hypertension remains unknown. Studies
evaluating a direct effect of EPO on the vasculature, as well as
indirect effects of increased hematocrit, viscosity and various humoral
substances have failed to yield a satisfactory mechanism to explain
EPO-induced hypertension.
In this study Hand et al hypothesize
that the treatment with EPO alters vascular responsiveness to
catecholeamines in hemodialysis patients leading to hypertension. They
evaluated the forearm vascular response to norepinephrine and
endothelin-1 in 9 consecutive ESRD patients (on maintenance hemodialysis
for at least 3 months) before and after 12 weeks of EPO. Hematocrit,
blood pressure and total peripheral resistance increased significantly
after EPO. Forearm vascular resistance response to intraarterial
norepinephrine was reduced as compared to healthy controls at baseline,
but increased significantly after 6 and 12 weeks of EPO. In contrast
the forearm vascular resistance response to endothelin-1 was decreased
although not significantly after EPO treatment.
The findings
indicate that vascular responsiveness to norepinephrine in anemic
hemodialysis patients is abnormally reduced and is restored after EPO
therapy and suggest that blood pressure elevation during EPO may be
mediated in part through this mechanism. This is an interesting
finding. If it is true that an increase in responsiveness to
norepinephrine points to the mechanism of EPO-induced hypertension, it
would be reasonable to test this hypothesis by use of clonidine or an
alpha-blocker as a means of controlling or preventing hypertension in
susceptible individuals.
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