From the Clinical Research Center, Vanderbilt University, Nashville,
Tenn.
Correspondence to Italo Biaggioni, MD, Clinical Research Center, AA3228 MCN, Vanderbilt University, Nashville, TN 37232-2195. E-mail italo.biaggioni{at}mcmail.vanderbilt.edu
AbstractVasodilation is one of the
most prominent effects of adenosine and one of the first to be
recognized, but its mechanism of action is not completely understood.
In particular, there is conflicting information about the potential
contribution of endothelial factors. The purpose of
this study was to explore the role of nitric oxide in the vasodilatory
effect of adenosine. Forearm blood flow responses to
intrabrachial adenosine infusion (125 µg/min) were assessed
with venous occlusion plethysmography during intrabrachial infusion of
saline or the nitric oxide synthase inhibitor
NG-monomethyl-L-arginine
(L-NMMA) (12.5 mg/min). Intrabrachial infusions of acetylcholine (50
µg/min) and nitroprusside (3 µg/min) were used as a positive and
negative control, respectively. These doses were chosen to produce
comparable levels of vasodilation. In a separate study, a second saline
infusion was administered instead of L-NMMA to rule out time-related
effects. As expected, pretreatment with L-NMMA reduced
acetylcholine-induced vasodilation; 50 µg/min acetylcholine increased
forearm blood flow by 150±43% and 51±12% during saline and L-NMMA
infusion, respectively (P<.01, n=6). In contrast,
L-NMMA did not affect the increase in forearm blood flow produced by 3
µg/min nitroprusside (165±30% and 248±41% during saline and
L-NMMA, respectively) or adenosine (173±48% and 270±75%
during saline and L-NMMA, respectively). On the basis of our
observations, we conclude that adenosine-induced vasodilation
is not mediated by nitric oxide in the human forearm.
© 1998 American Heart Association, Inc.
Scientific Contributions
Role of Nitric Oxide in Adenosine-Induced Vasodilation in Humans
Key Words: adenosine blood flow nitric oxide vasodilation acetylcholine nitroprusside
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