ELUCIDATION OF MECHANISM UNDERLYING PEROXYNITRITE MEDIATED IMPAIRED RELAXATION IN THORACIC AORTA OF ARTHRITIC RATS
Journal Title: Pharma Science Monitor-An International Journal Pharmaceutical Sciences - Year 2010, Vol 1, Issue 2
Abstract
Rheumatoid arthritis is a systemic inflammatory disease associated with generation of oxidative stress that produced vascular dysfunction. ONOO- a cytotoxic free radical and potent vasorelaxant. The present study was undertaken to determine the mechanism underlying ONOO- induced vascular relaxation in rat aorta with probable mechanism involved in impaired relaxation in arthritic rat aorta. Arthritis was induced by CFA (6 mg/ml, i.d.). After precontraction of aortic strips by PE (10-5M), vasodilatory response to peroxynitrite was taken. The strip of aorta was incubated with various potassium channel blockers such as TEA (Ca2+ activated potassium channel blocker), Glibenclamide (selective ATP dependent potassium channel blocker), 4-AP (Voltage dependent potassium channel blocker), BaCl2 (Inwardly rectifying Potassium channel blocker) and Methylene blue (sGC blocker). ONOO- induced relaxation was impaired in arthritic compared to control rat aorta, suggested that vascular dysfunction in Arthritis. In presence of Methylene blue, significantly inhibited ONOO- induced relaxation in control and arthritic thoracic aorta, suggested the role of sGC in ONOO- induced relaxation. TEA (10mM) and 4-AP (10-5M) significantly inhibited ONOO- induced relaxation in both arthritic and control rat aorta. While in presence of glibenclamide (10-5M) and BaCl2 (0.1mM) ONOO- relaxation was unaltered indicates that ONOO- induced relaxation may be via KCa and KV channel but independent of KATP and Kir channels. ONOO- induced relaxation involves activation of sGC and potassium channel particularly through KCa and KV channel. In arthritic rat aorta, impairment of ONOO- induced relaxation due to dysfunction in KCa and KV channels.
Authors and Affiliations
Panchal Aashish H. * , Patel Natvar J. , Patel Nailesh G , Vyas Amit S , Patel Rameshwar K. , Patel Madhabhai M
Keywords
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