Role of Endothelial-Derived Reactive Oxygen Species and Nitric Oxide in Norepinephrine-Induced Rat Aortic Ring Contractions

Author： Srivastava P. Hegde L.G. Patnaik G.K. Dikshit M.

Publisher： Academic Press

ISSN： 1043-6618

Source： Pharmacological Research, Vol.38, Iss.4, 1998-09, pp. : 265-274

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Abstract

In the present investigation involvement of endothelial-derived reactive oxygen species (ROS) and their interaction with nitric oxide (NO), during norepinephrine (NE)-induced contraction of rat aortic rings was studied. NE (1×10^-10 m to 1×10^-5 m) caused concentration-dependent contractio n of the endothelium intact aortic rings. In the presence of hydroxyl radical scavengers, histidine (1×10^-3 m), mannitol (3×10^-3 m), dimethyl sulfoxide (50×10^-3 m) or thiourea (1×10^-3 m), superoxide dismutase (superoxide radical scavenger, SOD 10 or 100 U ml^-1) or catalase (hydrogen peroxide inactivator 3, 10, or 100 U ml^-1) the concentration–response curve of NE was shifted towards the right. Interestingly, in N^G-nitro-l-arginine methyl ester (l-NAME) (1×10^-5 m, a NO synthase inhibitor) pretreated rings, NE-induced contractions were not inhibited by SOD or extracellular hydroxyl radical scavengers (mannitol and histidine). However, in these rings NE-induced contractions were found to be attenuated by endogenous hydroxyl radical scavengers (thiourea and DMSO) or catalase. In the endothelium denuded rings no significant effect of these scavengers on NE-induced contractions was observed. These results thus indicate the involvement of endothelium-derived hydrogen peroxide, superoxide and hydroxyl radicals in the NE-induced contractions. In addition, endothelial NO interacts with the ROS generated during rat aortic ring contractions.