(Hypertension. 2001;37:703.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
Potentiation of Bradykinin by Angiotensin-(1-7) on Arterioles of Spontaneously Hypertensive Rats Studied In Vivo
From the Department of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil, and the Department of Physiology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil (R.A.S.S.).
Correspondence to Maria Helena Catelli de Carvalho, PhD, Avenue Prof Lineu Prestes, 1524, sala 217, Cidade Universitaria CEP 05508-900 Sao Paulo, SP, Brazil. E-mail mahecaca{at}icb.usp.br
In
the present study, we investigated the potentiating effect of
angiotensin-(1-7) [Ang-(1-7)] on bradykinin (BK)-induced
vasodilation in the mesenteric vascular bed of anesthetized
spontaneously hypertensive rats using intravital microscopy. Topical
application of BK and Ang-(1-7) induced vasodilation in mesenteric
arterioles. The BK-induced effect, but not acetylcholine, sodium
nitroprusside, or histamine responses, was potentiated in the presence
of Ang-(1-7). This interaction was abolished by
BK-B2 and Ang-(1-7) antagonists (HOE
140 and A-779, respectively), a K+ channel
blocker (tetraethylammonium), and
cyclooxygenase inhibitors
(indomethacin and diclofenac); however, nitric oxide
synthase inhibition
(N
-nitro-L-arginine
methyl ester) did not modify the Ang-(1-7)–potentiating activity.
Long-term angiotensin-converting enzyme (ACE)
inhibition increased BK and Ang-(1-7)–induced vasodilation. The BK
potentiation by Ang-(1-7) was preserved after ACE inhibition, Ang II
type 1 receptor blockade, or the combination of both treatments.
The most striking finding of this study was the unexpected observation
that the potentiation of BK vasodilation in spontaneously hypertensive
rats treated short- or long-term with ACE inhibitors was
reverted by the Ang-(1-7) antagonist A-779. Our results
unmasked a key role for an Ang-(1-7)–related mechanism in mediating BK
potentiation by ACE inhibitors.
Key Words: bradykinin • angiotensin • microcirculation • hypertension • angiotensin-converting enzyme • renin-angiotensin system
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