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New Product Research Laboratories II, Tokyo Research and Development Center, Daiichi Pharmaceutical Company, Edogawa-ku, Tokyo 134, Japan
To examine whether the bradykinin-nitric oxide
(NO) pathway directly participates in the antihypertrophic property of
angiotensin-converting enzyme (ACE) inhibitors in congestive heart
failure, the effects of bradykinin were studied in rat cultured heart
cells. Bradykinin (0.1, 1 nM) prevented the phenylephrine-induced
increase in protein/DNA content, an index of hypertrophy of heart
cells, and amplified the nitrite/nitrate content in the medium.
Perindoprilat (1 µM), an ACE inhibitor, also restrained the
progression of cardiac hypertrophy and augmented NO release. These
effects of perindoprilat were abolished by HOE-140 (kinin
B2 antagonist),
N
-nitro-L-arginine
(NO synthase inhibitor), and methylene blue (guanylate cyclase
inhibitor). Furthermore, there was a significant correlation between
protein/DNA content and nitrite/nitrate content. These results
indicate that bradykinin inhibits the progression of cardiac
hypertrophy due to the increase in NO release and that perindoprilat
produces beneficial effects on cardiac hypertrophy by stimulating
the bradykinin-NO pathway.
rat neonatal cardiomyocytes; nitric oxide; perindopril
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