Modulation by bradykinin and nitric oxide of angiotensin II-induced apoptosis in a vascular smooth muscle cell phenotype

There is evidence for a clinical benefit of ACE inhibitors or AT1 antagonists in cardiovascular diseases with deleterious smooth muscle cells (SMC) apoptosis. We have previously shown that angiotensin II (Ang II) induces a phenotype-dependent SMC apoptosis. We asked whether bradykinin (BK) and nitri...

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Bibliographic Details
Published in:International immunopharmacology 2008-02, Vol.8 (2), p.231-236
Main Authors: Colie, S., Pecher, C., Girolami, J.P., Blaes, N.
Format: Article
Language:English
Subjects:
Angiotensin II
Angiotensin II - pharmacology
Animals
Apoptosis
Apoptosis - drug effects
Bradykinin
Bradykinin - pharmacology
Cell Survival
Cell Survival - drug effects
KKS
Muscle, Smooth, Vascular
Muscle, Smooth, Vascular - cytology
Muscle, Smooth, Vascular - drug effects
Nitric Oxide
Nitric Oxide - physiology
Nitroprusside
Nitroprusside - pharmacology
Phenotype
RAS
Rats
Rats, Wistar
Survival
VSMC
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Summary:There is evidence for a clinical benefit of ACE inhibitors or AT1 antagonists in cardiovascular diseases with deleterious smooth muscle cells (SMC) apoptosis. We have previously shown that angiotensin II (Ang II) induces a phenotype-dependent SMC apoptosis. We asked whether bradykinin (BK) and nitric oxide (NO) could modulate Ang II-induced SMC apoptosis. BK alone did not induce significant apoptosis in either spindle (Sp-SMC) or epithelioid (Ep-SMC) SMC phenotypes cultured in serum reduction, but phenotype-dependently, reduced cell proliferation. Pretreatment with BK partly impaired Ang II-induced reduction of Ep-SMC culture viability and partly prevented apoptotic features. Pretreatment with sodium nitroprusside completely prevented all Ang II-induced deleterious effects in Ep-SMC, i. e. reduction of culture viability, Annexin V binding, nuclear condensation and cell fragmentation. These findings indicate that the BK–NO system may phenotype-dependently modulate SMC survival and in particular may oppose, mostly by NO, Ang II-induction of apoptosis in the Ep-SMC phenotype.
ISSN:1567-5769
1878-1705
DOI:10.1016/j.intimp.2007.09.006