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Vol. 286, Issue 1, 403-410, July 1998
Hypertension and Vascular Research Division, Heart and Vascular
Institute, Henry Ford Hospital, Detroit, Michigan
Angiotensin 1-7 (Ang 1-7) has been reported to induce relaxation
which is partially blocked by a kinin receptor antagonist. We
investigated the relationship between kinins and angiotensin peptides
with use of preconstricted isolated pig coronary arteries. Ang 1-7
alone (up to 10
M) had no relaxant effect.
Bradykinin (BK)
(10-10 M)
induced transient relaxation, returning to basal tone, although BK
remained in the bath. In these BK-stimulated rings, Ang 1-7 but not BK
(both 5 × 10 M) again relaxed the
rings by approximately 50%. This relaxation was blocked by a BK
B2 antagonist, a kininase, and a nitric oxide synthase
inhibitor. Ang 1-7 inhibited purified angiotensin-converting enzyme
(ACE) by 30 ± 3.5% (n = 4) at
10 M. However, in BK-pretreated rings, the
ACE inhibitor ramiprilat did not induce relaxation, nor did it affect
the relaxant response to Ang 1-7, which suggests that the effect of
Ang 1-7 was not caused by ACE inhibition. Ang 1-7-induced
vasodilation was reduced by 69.9 ± 6.2% by an AT2
receptor blocker, PD-123319, and 29.3 ± 7.3% by an
AT1 antagonist, losartan. Neither the nonselective AT1/AT2 receptor antagonist sarthran nor
saralasin inhibited the response to Ang 1-7. Ang II did not elicit
relaxation either alone or in the presence of losartan, which suggests
that activation of AT2 receptors does not cause relaxation.
Thus, in the presence of bradykinin, Ang 1-7 relaxes pig coronary
arteries via a PD-123319-sensitive mechanism involving
nitric oxide, kinins and the BK B2 receptor. The
kallikrein-kinin and renin-angiotensin systems may be linked through
the interaction of Ang 1-7 and BK.
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