(Hypertension. 2000;35:998.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
From the Department of Medicine II, Yokohama City University School of Medicine, Yokohama, Japan.
Correspondence to Dr Shinichiro Ueda, Human Vascular Research Laboratory, Department of Medicine, Yokohama City University School of Medicine, 3-9, Fuku-ura, Kanazawa-ku, Yokohama 236-0004 Japan. E-mail sueda{at}med.yokohama-cu.ac.jp
AbstractAngiotensin-(1-7)
has been suggested to be a novel vasodilating peptide. We investigated
the direct vascular effect of angiotensin-(1-7) in human
forearm resistant vessels, particularly with regard to the
interaction with angiotensin II, in healthy normotensive
men by strain-gauge venous occlusion plethysmography with
intra-arterial infusions of peptides.
Intra-arterial infusion of angiotensin-(1-7) at
0.1 to 2000 pmol/min did not cause vasodilatation but rather reduced
forearm blood flow by
10% at the highest dose. A placebo-controlled
study showed that angiotensin-(1-7) at 0.5 to 40 nmol/min
caused weak but significant vasoconstriction (P=0.0016
by ANOVA). Angiotensin-(1-7) at 100 pmol/min, but not at 10
pmol/min, significantly shifted the angiotensin II
dose-response curve toward the right (mean±SD of percent changes in
forearm blood flow: -19±17%, -33±22%, -55±12%, -63±10%, and
-68±5% at 5, 10, 25, 50, and 100 pmol/min of angiotensin
II, respectively, with saline; 5±13%, 0.9±18%, -40±16%,
-54±9%, and -61±6% with angiotensin-(1-7),
P=0.0021 by ANOVA). Angiotensin-(1-7) did
not affect the dose-response curve of noradrenaline
[3±12%, 5±16%, -20±22%, -31±18%, and -40±12% at 25, 50,
100, 300, and 600 pmol/min of noradrenaline, respectively,
with saline; -4±15%, -2±23%, -29±22%, -34±16%, and
-42±9% with angiotensin-(1-7)]. Our results suggest
that angiotensin-(1-7) antagonizes vasoconstriction by
angiotensin II in human resistant vessels and might
act as an endogenous angiotensin II
antagonist.
Key Words: angiotensin angiotensin II noradrenaline blood flow velocity
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