Renin and angiotensin-converting enzyme (ACE) as active components of the local synovial renin-angiotensin system in rheumatoid arthritis

Local functional renin-angiotensin systems (RAS) have been demonstrated in many organ and tissue systems. Angiotensins, the effector growth factors of the RAS, are essentially cytokines and growth factors which actively contribute to many inflammatory reactions. Among the components of RAS, angioten...

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Veröffentlicht in:Rheumatology international 2005-05, Vol.25 (4), p.285-291
Hauptverfasser: COBANKARA, Veli, ÖZTÜRK, Mehmet Akif, KIRAZ, Sedat, ERTENLI, Ihsan, HAZNEDAROGLU, Ibrahim C, PAY, Salih, CALGÜNERI, Meral
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Sprache:eng
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Zusammenfassung:Local functional renin-angiotensin systems (RAS) have been demonstrated in many organ and tissue systems. Angiotensins, the effector growth factors of the RAS, are essentially cytokines and growth factors which actively contribute to many inflammatory reactions. Among the components of RAS, angiotensin-converting enzyme (ACE) and renin have been previously investigated separately in RA. In this study, ACE levels and renin concentrations were measured in the sera of 16 patients with RA (median age: 45 (26-69), male/female: 3/13), 13 patients with osteoarthritis (OA) (median age: 55 (28-72), male/female: 5/8), and 11 healthy adults (median age: 44 (35-70), male/female: 6/5). Synovial ACE levels and renin concentrations were also measured concurrently in patients with RA and OA. Serum ACE levels were comparable between the groups. However, synovial fluid ACE levels were significantly higher in the patients with RA than in patients with OA. Likewise, synovial fluid renin concentrations were higher in RA patients than in OA patients, while serum renin concentrations were similar in patients with RA and OA and in healthy controls. Moreover, there was a significant negative correlation between the duration of the disease and synovial renin concentrations in RA patients. In conclusion, locally-generated active renin and ACE could contribute to joint destruction in rheumatoid arthritis.
ISSN:0172-8172
1437-160X
DOI:10.1007/s00296-004-0564-8