Abstract | BACKGROUND:
Angiotensin-converting enzyme inhibitors (ACE-I) protect against the development of glomerulosclerosis using mechanisms partly dissociated from their systemic antihypertensive action. The aim of the current study was to delineate the mechanism of action underlying the antifibrotic effects of the ACE-I perindoprilat in the context of macrophage-mediated scarring in human mesangial cells. METHODS: RESULTS: CONCLUSION: These results suggest that ACE-I-induced renoprotection, in the context of macrophage-stimulated mesangial cell scarring, is mediated, at least in part, via the actions of bradykinin.
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Authors | Izabella Z A Pawluczyk, Samita R Patel, Kevin P G Harris |
Journal | Kidney international
(Kidney Int)
Vol. 65
Issue 4
Pg. 1240-51
(Apr 2004)
ISSN: 0085-2538 [Print] United States |
PMID | 15086463
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Angiotensin-Converting Enzyme Inhibitors
- Bradykinin B2 Receptor Antagonists
- Fibronectins
- Indoles
- Receptor, Bradykinin B2
- perindoprilat
- icatibant
- Plasminogen Activators
- Tissue Plasminogen Activator
- Bradykinin
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Topics |
- Angiotensin-Converting Enzyme Inhibitors
(pharmacology)
- Bradykinin
(analogs & derivatives, pharmacology, physiology)
- Bradykinin B2 Receptor Antagonists
- Cells, Cultured
- Fibronectins
(biosynthesis, metabolism)
- Fibrosis
- Glomerular Mesangium
(drug effects, metabolism, pathology)
- Humans
- Indoles
(pharmacology)
- Kallikrein-Kinin System
(physiology)
- Plasminogen Activators
(metabolism)
- Receptor, Bradykinin B2
(metabolism)
- Renin-Angiotensin System
(physiology)
- Tissue Plasminogen Activator
(metabolism)
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