مرکز منطقه ای اطلاع رساني علوم و فناوري -

چكيده لاتين :

Angiotensin converting enzyme (ACE) upregu-lation in stromal cells of joints affected by rheumatoid arthritis may lead to higher tissue angiotensin II that is a vasoconstric-tor and mitogen factor. To date, the role of angiotensin II on regulating blood flow in inflamed joints has not been studied. Methods: Acute and chronic joint inflammation was induced in rabbits by intra-articular injection of carrageenan and anti-gen-induced arthritis method, respectively. The ACE level of synovial fluid and the response of joint blood flow to angio-tensin II, angiotensin II receptor antagonist, and the role of nitric oxide (NO) in modulation of the effects of angiotensin II on joint blood vessels were examined. Results: The synovial fluid level of ACE was significantly in-creased during the process of inflammation and angiotensin II increased joint vascular resistance dose-dependently in both acute and chronically inflamed joints. The angiotensin 1 receptor an-tagonist losartan completely blocked the vasoconstrictor effect of angiotensin II on joint blood vessels and induced vasodilatation. Nitric oxide synthase inhibitor N-omega -nitro L- arginine methyl ester (L-NAME) increased joint vascular resistance and augmented vascular response of inflamed joints to angiotensin II. Conclusion: Angiotensin II receptors in joint blood vessels are angiotensin -1 subtype, and inflammation significantly increases the activity of synovial fluid ACE. Nitric oxide plays a significant role on regulating joint blood flow and in modu-lation of angiotensin 1 receptor-mediated vasoconstriction of inflamed joint blood vessels. Iran J Med Sci 2009; 34(1): 36-45.