Relaxation induced by histamine is not endothelium dependent in tail arteries of L-NAME-treated rats

The present study was carried out to evaluate the relaxation induced by his tamine in tail arteries of rats after chronic inhibition of nitric oxide (N O) synthesis with the inhibitor N-G-nitro-L-arginine methyl ester (L-NAME) compared to tail arteries of control rats. The maximum relaxation induced b y histamine was greater in control (88.09% +/- 5.50, n = 6) than in L-NAME arteries (47.33% +/- 6.40, n = 6), although pD(2) values were not different between the two groups (control: 4.89 +/- 0.08; L-NAME: 4.81 +/- 0.10). Af ter incubation with 100 muM L-NAME in vitro, the maximum relaxation induced by histamine was only reduced in the control arteries (44.93% +/- 2.35, n = 6), whereas it had no effect on aortas of rats pretreated with this inhib itor. The incubation with 100 muM L-NAME had the same effect as endothelium removal in both arterial groups. Furthermore, the relaxation induced by hi stamine was unaffected by indomethacin. The combination of L-NAME and the h istamine antagonist cimetidine completely abolished the relaxation induced by histamine in both arterial groups. These results show that when NO synth esis is impaired, the relaxation induced by histamine is endothelium indepe ndent, and when NO-synthase is active, the relaxation involves both NO rele ased from endothelial cells and an endothelium-independent mechanism that i s sensitive to cimetidine. (C) 2001 Elsevier Science Inc, All rights reserv ed.