In quiescent aortic spiral preparation of rat, hydrogen peroxide (H2O2) in concentration range of 10-6 to 10-3 caused the contraction of aortic spiral preparation dose dependently, while broad range of concentration caused triphasic response: a transient contraction (10-6-10-3 M) , relaxation (10-3-10-2.5 M) and persistence contraction (10-2 M). Endothelium removal potentiated the contractile response but did not affect the relaxant response suggesting relaxant response to H2O2 is independent of endothelium. Catalase (1000 U/ml), H2O2 scavenger, inhibit almost contractile as well as relaxant response, where as tempol (100 μM), superoxide anion scavenger and DMSO (dimethyl sulphoxide) (5 mM), hydroxyl radical scavenger, unable to inhibit contractile as well as relaxant response produced by H2O2, conforming the response is only due to H2O2 and not due to hydroxyl radical or superoxide anion. Genistein (100 μM), tyrosine kinase inhibitor, and verapamil (1 μM), voltage dependent Ca2+ channel blocker, inhibited contractile response whereas they could not inhibit the relaxant response. KCl (30 mM), potassium channel blocker, inhibits the relaxant response when added at the starting point of the relaxation, suggesting the role of the K+ channels in relaxant response to H2O2. TEA (tetra ethyl ammonium bromide- KCa blocker) (5 mM), 4-AP (5 mM), 4- amino pyridine, KV blocker and a KATP blocker Glybenclamide (10 μM), caused inhibition of relaxant phase but unable to potentiate or diminish contractile phase. Where as BaCl2 (0.1 mM), inward rectifier K+ channel blocker, could not inhibit relaxant as well as contractile phase to H2O2. So it is reasonably to conclude that relaxation, found in triphasic responses of H2O2, is not dependent on endothelium and it is due to the activation of the potassium channels like KCa, KATP, KV.
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